The American Soybean Association encourages constructive comments on this 2nd edition of the Poultry Disease Handbook. students. Shane < sshane@nc. and avian health professionals to diagnose.rr.com >
April. Most frequently. Careful evaluation of the history and application of modern techniques are necessary to diagnose and resolve complex infectious multi-factorial diseases. poultry organizations. some diseases such as avian influenza occur as epornitics. treat and prevent diseases in poultry flocks. Specialists and consultants affiliated to the American Soybean Association are willing to assist producers. and universities with additional information on specific aspects of the control and prevention of poultry disease. It is emphasized that in the context of Asia. production is impacted by combinations of infections and parasites which are invariably complicated by intercurrent nutritional. Simon M. 2005
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.PREFACE The second edition of the ASA Handbook on Poultry Diseases has been prepared for the American Soybean Association to assist veterinarians. cooperatives. including suggestions to be included in subsequent printings. environmental and managemental deficiencies.

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4. NUTRITION AND BIOSECURITY
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INTRODUCTION ECONOMIC CONSIDERATIONS IN THE PREVENTION AND CONTROL OF POULTRY DISEASES HEALTH AND PERFORMANCE OF POULTRY IN HOT CLIMATES PREVENTION OF DISEASE VACCINATION AND MEDICATION SPECIAL PROCEDURES RELATING TO CONTROL OF DISEASES IN POULTRY OPERATIONS NUTRITION OF CHICKENS AND DIETARY DEFICIENCIES
3.MANAGEMENT.0 2.0 6.

egg and laying strains have eliminated vertically-transmitted diseases from their elite and great-grandparent generations.1). These should incorporate projections of risk of infection and compare the production parameters and costs for diseased and healthy flocks. reoviral stunting syndrome and swollen head syndrome are examples of emerging diseases affecting flocks in Asia. highly pathogenic influenza. and Latin America. Prevention of disease depends on a comprehensive program incorporating a sequence of planning. Vaccination of parent flocks and progeny and appropriate levels of biosecurity represent the components of disease prevention subject to direct managemental control. pasteurellosis. reduces the potential losses caused by both catastrophic and erosive infections on commercial-scale farms. Improved biosecurity and an awareness of the need for appropriate vaccination programs. village cooperatives and in integrated operations. Unfortunately. vaccination. The relative importance and contribution of these strategies can be calculated using simulation studies.1. implementing and control in a repetitive cycle (Figure 1. Strategies to prevent infection are based on the purchase of breeding stock free of vertically-transmitted disease. and salmonellosis continue to erode profit margins. infection of grandparent and parent flocks occurs in many developing countries resulting in dissemination of diseases including mycoplasmosis.2):
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. and management. The components of biosecurity comprise a hierarchy with each of 3 levels influencing the cost and effectiveness of the entire program (Figure 1. Improving efficiency increases the availability of eggs and poultry meat to supply the protein needs of populations in countries with expanding demand. virulent infectious bursal disease. chronic. primary breeders of broiler. Angara disease. low-intensity infections such as coryza. During the past two decades. Africa.0
INTRODUCTION The purpose of the ASA Handbook on Poultry Diseases is to acquaint veterinarians and poultry health professionals with current information on the diagnosis and prevention of poultry disease in commercial broiler and egg production flocks in emerging and established industries. salmonellosis and reoviral infection. Productivity and profitability are enhanced by application of sound principles of biosecurity. In addition.

construction of drainage. bulk feed installations. defects in conceptual biosecurity cannot be changed in response to the emergence of new diseases which may result in severe losses or even failure of an enterprise.
•
•
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. and the interior finishes in houses. Siting of farms in relation to public roads and service facilities such as hatcheries. Generally. These activities can be modified at short notice to respond to disease emergencies. reduce biodensity. allweather roads.•
Conceptual Biosecurity: The primary level represents the basis of all programs to prevent disease. exclusion of rodents and wild birds. Structural biosecurity can be enhanced in the intermediate term with appropriate capital investment. Decisions concerning conceptual biosecurity influence all subsequent activities relating to prevention and control of disease. feed mills. change rooms. erection of fences. Conceptual biosecurity includes selecting the location of a complex or operation in a specific area to separate different types of poultry. and avoid contact with free-living birds. Remedial action may often be too late to respond to the emergence of a new disease or an epornitic of a catastrophic infection such as highly pathogenic avian influenza. Constant review of procedures. and processing plants has a profound impact on the effectiveness of a program to maintain optimal standards of production. equipment for decontamination. participation by all levels of management and labor and appropriate monitoring of the health status and immunity of flocks contributes to effective operational biosecurity. Operational Biosecurity: The third level comprises routine managemental procedures intended to prevent introduction and spread of infection within a complex or enterprise. Structural Biosecurity: The second level of biosecurity includes considerations such as the layout of farms.

It is therefore necessary to market poultry. If the NPV exceeds the cost of improvements. and eggs at a price which allows farmers or integrators to maintain profitability in a competitive market. derived from improved performance attributed to the absence of disease. There is considerable difficulty in predicting the potential loss arising from a disease or projecting the probability of an outbreak. where the prevalence of endemic diseases severely affects production efficiency or where the value of eggs and meat is high in relation to expenditure on biosecurity and vaccination. The benefit-to-cost ratio can be used to relate expenditure on resources and management efforts to the monetary value of improved performance. It is emphasized that the incremental return in the form of enhanced egg production. Aggressive counter measures are required under conditions which predispose to a high risk of infection. Changing rooms. Programs of emergency treatment and long-term prevention are justified for severe diseases which have a profound impact on production.0
ECONOMIC CONSIDERATIONS IN THE PREVENTION AND CONTROL OF POULTRY DISEASES General Principles The primary purpose of any enterprise is to maximize return on investment over the long-term. are the two significant variables required to quantify the decline in production which may follow exposure to a disease. fences and equipment to decontaminate hatcheries and housing are examples of assets which reduce the probability of introducing disease.2. discounted by an appropriate interest factor. should be calculated for a period corresponding to the operating life of the investment. The future cash flows. The NPV method can be used to select the most beneficial program to prevent disease from among
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2. liveability. A decision to invest in improvements which promote biosecurity should be based on an anticipation of return within a defined. Cost-effective programs of biosecurity and vaccination are required to prevent or limit the impact of disease. Risk of exposure and consequences of infection.1
. meat products. and feed conversion efficiency must exceed capital and operating expenditures on disease prevention. the investment can be considered justifiable. growth rate. hatchability. The net present value (NPV) of an investment in biosecurity can be calculated from the annual cash flows. It is necessary to invest capital in adequate poultry housing and ancillary installations to attain a suitable level of biosecurity. and preferably short to intermediate time period.

which benefits progressive integrations and cooperatives in mature industries. Offsetting fixed costs by increasing production level is the basis of efficiency through economy of scale. The concept of apportioning expenditure is important in projecting the effects of disease on total production cost. there are limits to increasing production volume. Implementing these management changes will increase the risk of disease and intensify the financial impact of infections.95 kg) may increase biomass by 11%. purchase of day-old chicks and breeding stock. and lease payments. vaccines and medication. Feed.75 to 1. Fixed costs which are constant are illustrated by the line parallel to the horizontal (quantity) axis. Variable costs are proportional to the volume of production. Altering stocking density from 20 to 25 birds/m2 increases throughput by 25%. At this level of production fixed costs represent approximately half of the total cost. Total costs are represented by the area which encompasses both fixed and variable costs. overhead. are examples of this category of production costs. interest on fixed capital. Fixed costs do not change as a result of an increase in the volume of production and include depreciation. given prevailing production costs and revenue. packaging material.2 Fixed and Variable Costs in Poultry Production Costs relating to live bird production can be classified into fixed and variable components.1 shows the relationship between total cost. hatcheries. It is emphasized that the validity of any investment decision is dependent on selecting an appropriate value for the risk of infection and accurately projecting the consequences of disease. variable cost assumes a greater proportion of total cost. labor.a range of alternatives. In the context of individual farms. salaries. At the break-even point (quantity Qo) total revenue is numerically equal to total costs. unit selling price is considered constant over volume of throughput and accordingly revenue is linear and proportional to the quantity produced. The severity of viral respiratory diseases such as bronchitis or
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. Delaying slaughter of a broiler flock to attain a higher live mass (1. A decrease in broiler weight delivered to a plant attributed to increased mortality or depressed growth rate will adversely affect production cost and efficiency. 2. At a higher throughput. Figure 2. volume of production and profit. Processing plants. Reducing intercrop interval from 10 to 5 days may result in an 8% increase in broiler live mass over a year. In this example. fuel. and feed mills operate at a break-even cost approximating 70% to 80% of design capacity due to their relatively high proportion of fixed costs.

costing $2. A series of analyses can be performed reflecting alternative prevention strategies and probabilities of disease exposure. The effect of intercurrent low-grade conditions such as pasteurellosis. The values calculated from the gross marginal analysis are entered into a pay-off table which depicts the financial result of a selected option. Expected monetary values are influenced by changes in variable costs. The inputs required to determine the gross margin attributable to a specific program are listed for an ongoing poultry operation over a specific time period.800 for no action.400.000 and $5.6 probability of occurrence. The format table for gross marginal analysis is shown in Figure 2. mycoplasmosis or coccidiosis may be exacerbated by increased biodensity. feeding space. Figure 2. unit revenue. and the probability of infection. biosecurity (#1) or vaccination (#2). Secondary infections such as E.3 Gross Marginal Analysis This analytical technique can be applied to relate expenditure on disease prevention with output over a specific time period. The corresponding gross margins generated when flocks are subjected to either biosecurity alone (strategy #1) or vaccination alone (strategy #2) can be calculated and entered into a pay-off table. 2.000 with and without exposure to disease.2. Gross marginal analysis allows producers to project the possible outcome of a program with uncertain risks and consequences of infection.3 considers the effect of three alternative approaches to preventing a disease which has a 0. It is determined that the respective gross margins derived from the flock under conditions of no action are $3.460 for increased biosecurity. The expected monetary value of each prevention strategy is calculated by multiplying the probability factor with outcome as shown.000 and $10. The technique evaluates alternative methods of preventing disease in the context of prevailing costs and revenue. coli septicemia will intensify losses in proportion to increased biomass. Ventilation.000 provides the highest of $8. drinking points and floor area represent the limiting health factors for flocks when output is increased. capacity. The options available to the producer include: no action (“base = 0”). Variability in the impact of a disease occurs due to change in the pathogenicity of the causal organism. the presence of secondary agents. Changes in these factors influence the outcome of exposure of a flock to infection and requires relaxation or intensification of the preventive strategy depending on the
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. vaccination costing $1. immuno-suppression or environmental stress. In the given example.laryngotracheitis is influenced by environmental and clinical stress. compared to $6.

As expenditure on control of velogenic Newcastle disease (vvND) or highly pathogenic avian influenza (HPAI) by effective vaccination is increased. Figure 2. such as intensifying the vaccination program and implementing biosecurity will result in an incremental reduction of losses.
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. Increased outlay on disease prevention and control. such as the need to eradicate a vertically transmitted infection in breeding stock or to suppress a disease of zoonotic significance. control measures are extended beyond the economic optimum. At this point additional efforts to prevent disease will not achieve any measurable reduction in losses. and injection of embryos and chicks with mycoplasmacidal drugs. This sequence may be illustrated by the intensive programs to eradicate mycoplasmosis by the primary broiler breeders during the 1960’s and 1970’s. Under certain conditions. Additional prevention and control activities will in fact reduce gross margin and generate a negative benefit:cost ratio. Ultimately the technical optimum (B) is attained.4 depicting expenditure and return from control of disease shows the relationship between expenditure on prevention and control measures (horizontal axis) and the loss associated with introduction of disease (vertical axis). the loss in output is reduced. These measures together with pre-incubation heattreatment of eggs to destroy Mycoplasma spp and enhanced biosecurity and monitoring of pure-line flocks maintained in strictly-isolated small groups eradicated the disease in elite lines. The low cost of ND and HPAI vaccination and the relative efficiency in improving liveability and enhancing the growth rate or egg production in infected survivors reduces losses associated with minimal expenditure as designated by the curve LoL1.circumstances. Control measures included pressure-differential treatment of eggs with antibiotics. Eventually the economic optimum is reached (point A) at which a monetary unit of expenditure on control generates only a single unit of return.

(4)]
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.2 GENERAL FORMAT FOR GROSS MARGIN ANALYSIS
(1) (2) (3) (4) (5) (6) (7) (8) (9)
Value of inventory at the beginning of the period Cost of chicks/flocks purchased Variable costs (feed. management.1 CONCEPTUAL RELATIONSHIP BETWEEN COST AND REVENUE
FIGURE 2. health care) Total value at the beginning of the period plus all costs [ (1) + (2) + (3) ] Value of flock at the end of the period Value of chickens and products sold Revenue from by-products Total value at the end of the period [ (5) + (6) + (7) ] Gross margin [ (8) .FIGURE 2.

FIGURE 2.4 RELATIONSHIP BETWEEN EXPENDITURE AND RETURN FROM DISEASE CONTROL
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chickens are almost entirely dependent on latent heat loss for thermoregulation. This effect is mediated through T-cell or regulatory amplifier cell response. reducing antibody titer. Houses should be oriented in an east-west direction to limit solar heat load.0
HEALTH AND PERFORMANCE OF POULTRY IN HOT CLIMATES Physiological Effects of High Ambient Temperature Exposure of poultry flocks to ambient temperature above the zone of minimum metabolism results in an increase in endogenous heat production. and insulation. provision of adequate air inlets. Structures should be designed to permit passive airflow over the flock.8 m to limit solar gain through the side walls. and the interior height at the apex should not be less than 4 m to reduce air temperature at bird level. Respiratory rate can increase from 22 breaths/minute (bpm) to 200 bpm when ambient temperature is increased from 27ºC to 45ºC within 20 minutes.3. Convective transfer of heat is the major thermo-regulatory mechanism of chickens and depends on movement of air by natural or fan-powered ventilation. Cellular immunity is also suppressed by prolonged exposure to temperatures in excess of 36ºC. Prolonged hyperpnea results in excessive excretion of carbon dioxide resulting in respiratory alkalosis. Roof overhang should extend at least 0. egg production.1
3. The significant design characteristics for convection-ventilated houses relate to internal dimensions. Exposure to high ambient temperature has a profound economic impact on liveability. and above 38ºC. Convection houses should not exceed 10 m in width to facilitate cross flow of air at low velocity. An increase in convective heat transfer as a result of air movement is proportional to air velocity of up to 100 m/minute. and feed conversion efficiency. provided ambient air temperature is below body temperature. The lateral ventilation openings should comprise at least 60% of the side
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. egg shell quality.
3. growth rate.2
Design of Housing in Tropical Countries Convection-ventilated housing is most frequently used in temperate and tropical areas where moderately high seasonal temperatures occur. Size and siting of houses in relation to local topography are critical to achieving satisfactory results. Exposure to high environmental temperature for extended periods will suppress the humoral immune response of chickens. It is presumed that a reduction in circulating antibody is associated with a corticosteroid-induced change in serum ions. Hyperpnea (panting) occurs in mature chickens exposed to temperatures exceeding 30ºC. Panting facilitates evaporative cooling.

it is necessary to increase the rate of air movement in a house. Convention-ventilated houses are economically justified in many warmclimate areas with developing poultry industries. This can be achieved either by installing fans in closed housing or by selecting an appropriate configuration of air inlets in relation to the dimensions of convection-ventilated units.5m2 ºC/W (R = 14) and 1. The efficiency of this process is proportional to the velocity of the air stream and the temperature differential which exists between the bird and its surroundings.
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. but evaporative cooling can avert losses from heat prostration even in extremely hot and humid areas. mechanical ventilation is required. the area of the side opening can be controlled automatically by a thermostatically activated motorized winch with an emergency high temperature release mechanism in the event of power failure. Egg production. Simple mechanical and electrical installations and elementary technology for management and maintenance favor the basic convection-ventilated unit in tropical and subtropical areas. and heat content of air is depicted in psychometric charts. Air movement facilitates convective heat loss by the bird. All systems function on the principle of adiabatic cooling from a change of state of water from liquid to vapor. The physical relationship between dry bulb temperature. When daily ambient temperatures exceed 30ºC with any frequency. the relatively low capital and operating costs optimize profitability.2 m2 ºC/W (R = 7) for roof and wall structures respectively. relative humidity. In modern units.wall area and should be fitted with impervious curtains. General recommendations for insulation in tropical countries include values of 2. Generally. and feed conversion are improved in heat-stressed flocks provided with a direct stream of air. Evaporative cooling is used to reduce the severity of heat prostration in areas where the maximum temperature exceeds 35ºC with seasonal regularity. Although stocking density is generally low (eight to ten broilers or pullets or two to three mature breeders per square meter) compared with more advanced housing. To overcome high environmental temperatures. fertility. Fiberglass blanket insulation or polyurethane panels should be coated with a reflective radiant barrier of aluminum film on the exposed outer surface and should be provided with an impervious plastic protective lining for the inner surface. low humidity improves the efficiency of adiabatic cooling at high ambient temperature.

The simplest evaporative cooling system comprises fogger nozzles which deliver up to 8 to 10 l/hr at a pressure of 5 to 8 bar. and head exerts a cooling effect. Systems require frequent cleaning and descaling and litter becomes saturated in the vicinity of the nozzles. Insulation of header tanks and supply piping is indicated if the temperature of water at the point of consumption exceeds 25ºC.S.3 Management of Flocks at High Temperature The survival of birds at high temperature is strongly influenced by the volume of water consumed. commercial equipment functions with an efficiency ranging from 60 to 80%. This system is used in the U. low-pressure fogger nozzles are inefficient with respect to the cooling effect relative to water consumed. The efficiency of cooling may be enhanced by spraying pads with water from suitably placed nozzles. where seasonally high temperatures are encountered. Although systems are capable of achieving a 5ºC reduction in temperature with ambient air of 37ºC and 30% RH. The system should only be operated when humidity is below 70% RH and with fans displacing 5 m3/ hr per broiler. Nozzles are positioned in close proximity to turbulence fans to provide one discharge point for each 500 birds. Generally.Air at 45ºC and 15% RH could theoretically be cooled to 25ºC assuming complete saturation. Recommendations include 1 suspended drinker with a diameter of at least 40 cm. 3. and Latin America. where low cost is compatible with existing convection-ventilated houses.
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. the coarse-nozzle system is unsuitable in Middle Eastern countries due to inefficient utilization of scarce water and blockage of nozzles by mineral contaminants in artesian water. the U. Pad cooling systems are used extensively in Asia.A. The principal deficiency of the pad lies in the inherently lower efficiency of evaporation compared with the ultra-high pressure fogger.S. Modern cooling pads are composed of cellulose material in a honeycomb configuration to increase surface area. Although this enhances cooling. Cold water functions as a heat sink in the intestinal tract and surface evaporation from the comb. The low-pressure fogger nozzle produces a coarse spray. Due to restraints associated with the process of evaporation.. for 75 broilers or 50 breeders and 1 cup or nipple per cage of up to 5 commercial layers. the system is susceptible to algae and mineral contamination in water. wattles. It is essential to provide additional watering points to facilitate consumption in areas where ambient temperature exceeds 3º∫C for more than 2 hours per day. Air at 45ºC and 15% RH could be cooled to a dry bulb temperature of 30ºC with an elevation in relative humidity to 60%.

but feed conversion. and return were lower than with other combinations examined. drainage. The use of night feeding with a reversed lighting program (18:00 to 6:00) supported a significantly higher level of egg production than conventional daytime feeding.
1.Research on integrating lighting programs and operation of feeders for broilers has been reported from Singapore. concrete apron.
Convection ventilated broiler house on an island subject to hurricanes necessitates concrete construction. Note the relative size of ventilation
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Exterior of breeder house showing relative size of sidewall ventilation openings. This reverse diurnal lighting program produced the highest live weight at 56 days. Various lighting and feeding programs were investigated in Nigeria using medium-strain commercial layers. bulk-feed installation and grassed area surrounding the unit. which was accompanied by exposure to high diurnal temperature. mortality.
2. Performance was improved in convection-ventilated housing using nocturnal illumination and feeding.

consistent with health. Flock is uniform and well feathered for age.
Broilers showing signs of heat stress.
Interior of broiler house showing 2 rows of pan feeders and 4 rows of suspended plastic drinkers.3.
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5.
Equipment used to grow broiler chicks showing 20 year old overhead-filled pan feeding system and modern nipple-cup drinkers. Flock is uniform in size and shows feathering and pigmentation.
4.

Uniformity in flocks is achieved with adequate feeding space and a supply of clean water from a closed system through nipples or cups.
8.
Chicks beneath a gas-fueled pancake brooder show good distribution consistent with satisfactory growth and feed conversion efficiency.
Modern high-density cage installation with mechanical feeding and egg collection and fan-powered ventilation controlled by electronic systems.6.
7.
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Monitoring of atmospheric ammonia at litter level using a bellows pump and chemical indicator system which is sensitive to ammonia. High ammonia level results in respiratory stress and blindness. Fluorescent lamps require less electrical power than incandescent bulbs.
10.
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. Metal nest boxes with manual collection of eggs are easy to decontaminate. results in respiratory stress and causes severe reactions to aerosol vaccination and viral respiratory infection. Hens obtain feed from troughs fitted with male exclusion grills.
High level of dust due to inappropriate ventilation.
Breeder flock in convection-ventilated house showing ceiling insulation to reduce solar heat gain & belt-driven fan to create air movement over the flock. Vertical plywood boards prevent perching.
11. Suspended manual feeders for cockerels.9.

Pododermatitis (Bumble foot) resulting from wet litter.
Vent peck and disembowelment in cagehoused hens can be avoided by precision beak trimming at 7-10 days of age and adjusting light intensity to 20 lux.
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.12.
Keratitis (inflammation of the cornea) and conjunctivitis following exposure to high levels of atmospheric ammonia. Obese cockerels and hens are susceptible to this condition which reduces fertility.
14.
13.

4. laryngotracheitis and pasteurellosis.4.1 Transovarial Route Pathogens may be transmitted by the vertical route from hen to progeny via the egg.0
PREVENTION OF DISEASE Prevention of disease in commercial poultry operations requires the application of a coordinated program of biosecurity. wild birds. or dust carried by wind.1
Mechanisms of Disease Transmission In order to develop control procedures it is important to understand the mechanisms by which pathogens are introduced into commercial poultry farms and how disease agents are disseminated among units. equipment. This situation occurs in multiage units and is a common method of transmitting salmonellosis. pullorum disease (Salmonella pullorum). This form of vertical transmission results in contamination of the hatchery environment and direct and indirect infection of chicks.
4.3 Direct Transmission Contact between susceptible flocks and clinically affected or asymptomatic reservoirs of disease will result in infection. Biological transmission occurs when the pathogen multiplies in the infected host which then transmits the agent when placed in contact with susceptible flocks.1. mycoplasmosis.2 Transmission on the Egg Shell Pathogens such as E.1. Omphalitis and salmonellosis may be introduced into brooding and rearing units by contaminated egg-shells. rodents. 4. Salmonella enteritidis (Se) may also be transmitted vertically by incorporation of the bacterium into the albumen of the egg in the oviduct. Mechanical transmission involves transfer of a pathogen from an infected source or reservoir host to a susceptible flock by contaminated personnel.1.
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. coryza. The following mechanisms of transmission are recognized. coli and paratyphoid Salmonella spp deposited from the cloaca or nest-box litter can penetrate the shell and infect the developing embryo. vaccination and hygiene. Mycoplasmosis. 4. reoviruses and adenoviruses are transmitted in this way. insect vectors.

Argasid ticks (Argas spp) are vectors of spirochetosis. 4.4 Indirect Transmission Introduction of contaminated transport coops.5 Dissemination by Wind Infected flocks may excrete large numbers of viruses which can be entrained in dust and moved by wind for distances of up to 5km. or the agents responsible for chicken anemia and reticuloendotheliosis. 4.1. Sale of live poultry involves frequent visits to farms by dealers who ignore the most rudimentary biosecurity precautions. Insects are responsible for transmission of various diseases. and dealers in live poultry are significantly involved in transmitting disease. Pox.
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. Litter beetles (Alphitobius diaperinus) are reservoirs of a wide range of infections including Marek’s disease. Spread of vvND and ILT by wind has been documented in a number of outbreaks. House flies transmit campylobacteriosis.8 Vaccines Contaminated poultry vaccines prepared in eggs derived from non-specific pathogen free (SPF) flocks may contain pathogens including adenoviruses. reoviruses. West Nile and Highland J arbovirus may be transmitted by mosquitoes and spirochetosis by Argas ticks. Delivery of feed in bags requires manual handling. Rodents carry a wide range of diseases including pasteurellosis and salmonellosis.1. salmonellosis.7 Feed Contamination of ingredients or manufactured feed with pathogens such as Salmonella spp. 4. workers.4.1. 4. equipment or feed onto farms or movement of personnel between infected and susceptible flocks without appropriate biosecurity measures will effectively transmit disease. In the context of Asia. Imperfectly decontaminated buildings which have housed infected flocks often contain pathogens including infectious bursal disease virus (IBDV) and Salmonella spp which can infect successive placements especially when interflock intervals are less than 10 days in duration. supervisors. pasteurellosis and coccidiosis. IBD. or IBD and paramyxovirus virus can result in infection of susceptible flocks.1. Pathogens may also be transmitted among flocks as a result of contaminated vaccination equipment or personnel used to administer vaccines.6 Biological Vectors Wild birds are reservoirs of avian influenza and Pasteurella spp.1.

• All-weather roads within secured perimeter to facilitate cleaning and to prevent dissemination of disease agents by vehicles and footwear.2 Structural Biosecurity • Fenced farm area with notices to prevent trespass. • Concrete apron with a suitable water and power supply to permit decontamination of vehicles entering the farm. A successful biosecurity program presumes an understanding of the principles of epidemiology and economics and requires teamwork to maximize benefits. and change roomshower facilities.2. • Implementing including erection of facilities. The following items should be considered in evaluating a comprehensive biosecurity program for a breeder or growout complex:
4. with secured gates.
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.2
Biosecurity Evaluating the biosecurity of ongoing operations is important in developing effective programs to prevent the introduction of disease into a complex or to limit subsequent dissemination among farms. • Appropriate location of bulk bins or secure. vermin-free storage areas for bagged feed.2. • Location of major and minor roads and the movement of commercial and backyard poultry in relation to company facilities. • Distance among breeder and growout farms and facilities such as hatcheries. and processing plants or packing units. • Fencing of house area. • Installations for disposal of dead birds (incinerators.4. • Water supply free of pathogenic bacteria. pits). company-owned or contractor-operated facilities. • For commercial egg production consider the implications of multi-age on-line units or single-age. 4. and chlorinated to a level of 2 ppm. storage.1 Conceptual Biosecurity • Location of the complex in relation to concentrations of poultry of the same or different species. • Proximity to large lakes or waterways or migratory flyways. • Farm service module comprising an office. • Locating resources and training of personnel. feed mills. composters. • Control involving review of results and analytical procedures. Biosecurity programs require a structured approach involving the following sequence: • Planning and evaluation of programs.

• Concrete floors for breeding stock at the grandparent level. In many countries with endemic salmonellosis. o Storage. o Controls required to prevent contact with exotic avian species. supervisors. reconstitution and administration of vaccines according to recommended route. unused litter and cleaned equipment should be stored in a module separated from the live-bird area of the house to prevent contamination of flocks by delivery and maintenance workers.
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. Manuals should be developed for appropriate levels of management including company veterinarians and health maintenance professionals. hatcheries. • Correct positioning of extractor fans to prevent airborne transmission of pathogens to flocks in adjacent houses. breeding and grow out facilities. and backyard poultry. • Standardized procedures should address specific aspects of operation including: o Decontamination and disinfection of units following depletion of flocks.3 Operational Biosecurity • Operational manuals should be developed for routine procedures carried out in feed mills.2. o Specific procedures on entering and leaving farms should be designated for managers. • Impervious apron adjacent to the door of each house and installation of drains. contractors. 4. work crews and permanent and part-time employees. authorized visitors. concrete floors are required in both rearing and laying housing for breeders.• Secure housing with appropriate bird and rodent proofing. service personnel. Manuals should incorporate contingency plans in the event of a deviation from normal production parameters or outbreaks of disease on company farms or in units located in close proximity to the operation. • Feed. and employees.

15.
Structured post-mortem examination is necessary to determine the presence of lesions characteristic of a disease in the flock.
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.
16. Pathologists should take precautions to prevent personal infection and should exercise high standards of biosecurity to obviate transmission of pathogens.
Clinical examination as part of a disease investigation requires evaluation of representative birds from a flock to determine the organ systems which are involved.

These compounds should not be used in the presence of live poultry.2 Decontamination Thorough decontamination is necessary to achieve effective disinfection.3
Decontamination of Housing and Equipment
4.
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. • Organic phenols are suitable for use in hatcheries to decontaminate equipment. derived from petroleum distillation are cheap and effective biocides when applied to buildings and soil. • Cresols. it is necessary to take into account the chemical characteristics. Cleaning programs require planning followed by implementation and control to ensure satisfactory preparation of surfaces for subsequent application of disinfectants. Use of formalin requires special precautions to avoid exposure and injury to applicators who must be provided with protective clothing. In selecting a disinfectant.5 to 7. Hypochlorite is only effective over a pH range of 6. eggs. • Chlorine compounds are widely used in processing plants and to purify water on farms.1 Definitions Decontamination is the process of physically removing biological and inorganic material from the surfaces of a building or equipment. 4.3 Disinfectants A number of compounds are available commercially.5 in water free of organic matter and requires 10 . Disinfection is the destruction of pathogenic organisms.3. and in hatcheries provided that an anionic detergent precedes application of a QAT. each with characteristics for specific applications. 4. functional equipment and chemical monitors. and the cost of application.4. • Quaternary ammonium compounds (QATs) are highly recommended to decontaminate housing. equipment.3.20 minutes exposure to inactive bacteria • Formalin is a corrosive and potentially carcinogenic compound suitable to fumigate eggs in purpose-designed cabinets.3. toxicity. or processed meat as tainting of products will occur.

Detergent should be applied to the exterior in the sequence of roof. and service areas.4 Disinfection of Poultry Houses Complete depopulation of houses and decontamination of units and surroundings at the end of each broiler. • The floor of the house should be swept to remove residual litter. and products.4. rearing. • The surface of the litter and the lower side walls should be sprayed with a 2% carbamate insecticide. internal walls. • Litter should be graded to the center of the house for removal either manually or with a front-end loader.4 Public Health Considerations In most countries the use of disinfectants and pesticides is controlled by legislation which restricts the use of products to specified and approved application in accordance with manufacturers’ label directions. breeder or layer cycle will contribute to enhanced liveability and performance in subsequent flocks. the US Department of Agriculture and the US Food and Drug Administration guidelines are recommended. • The interior structure and equipment should be rinsed with water and remaining detergent solution should be allowed to drain. 4. • The house should be decontaminated by spraying a non-ionic detergent at a concentration recommended by the supplier. drains. • The interior of the house should then be sprayed with a quaternary ammonium or phenolic disinfectant solution at a concentration recommended by the manufacturer. exterior walls. and switch gear should be cleaned using a high-pressure air spray and then sealed to protect installations from water damage. A cresolic disinfectant can be applied to earth floors.3. Litter should be either bagged or alternatively transported in bulk from the house to a central site for composting or disposal. and then the floor.
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. • Equipment should be disassembled and removed from the house for cleaning and disinfection. • Electrical units. Cleaning the interior should follow the sequence of ceiling. Recommendations concerning disinfection and pest control should always conform to statutory regulations and should be designed to limit possible contamination of the environment. The following procedures should be followed. flocks. motors. In the absence of national or local rules.

A quaternary ammonium compound (1 . Fresh droppings may be observed around the inner perimeter of the poultry house. sawdust) should be spread to a depth of 3 . (Alphitobius spp) • Equipment should be reassembled and routine preventative maintenance completed.10 cm. Rodents serve as mechanical transmitters of infectious agents such as influenza and infectious bursal disease viruses and Salmonella and Pasteurella spp. proportioned at 1%) should be used to flush water lines.
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. Colonization can be detected by the presence of active nesting sites in attics. in cracks in concrete slabs. Rodents are nocturnal and are active after lights have been turned off. under cages. switch gear. in corners. rice hulls. A fog generator can also be used to distribute formalin in aerosol form through the house. Rats and mice are seldom seen during the day unless infestation is very heavy. electrical cables.000 dilution) or chlorine solution (1 liter of 6% sodium hypochlorite per 8 liters of water as a stock solution. Salmonella typhimurium and S. or in burrows around the foundation walls. They cause damage to building structures. It is emphasized that formalin is a toxic compound and is potentially carcinogenic. (See 4. and insulation. including Pasteurella multocida.2.5 Control of Rodents Rats and mice are significant pests in poultry facilities. enteritidis. water lines. Outdoor burrows may be closed by filling with soil and observed for reopening of entrances. in manure. including foundations. Appropriate protective clothing and respirators should be used and workers should be trained to use the compound in accordance with accepted procedures to protect health. A clean. The frequency of catching rodents in traps may also be used to assess the level of infestation. • Rodent control measures should be implemented including sealing of burrows and baiting. groundnut hulls. over the floor area. dry substrate (wood shavings. and floor to control litter beetles.• A 2% carbamate insecticide solution should be sprayed on the ceiling. Rodents are major vectors and reservoirs of poultry and zoonotic pathogens. walls. • Water lines and drinkers should be drained and cleaned. • Breeder houses should be sealed and fumigated with formalin generated from heated paraformaldehyde or from a mixture of formaldehyde and potassium permanganate.5 below) 4. Mice amplify environmental contamination and will infect poultry and products.

6 Control of Free-Living Birds Free-living migratory and resident birds serve as reservoirs and disseminators of numerous infections of commercial poultry. but most available anticoagulant rodenticides require 4 to 7 days after ingestion. or in water. pets. All rodenticides are poisonous at various levels for poultry. Baits are available in dry or wet form. and manufacturer’s label instructions should be strictly followed. The rate of rodent kill depends on the type of rodenticide and the dose consumed. in paste. water. and humans. avian influenza. in pellets. micro-encapsulated. Rodenticides are available for single. A single-dose rodenticide will kill rodents after one feeding if an adequate amount is consumed. Preventing access to feed. and chemical and nonchemical elimination. and at the entrance to houses and near active burrows. For maximum effectiveness. in wax.A continuous integrated program to control rodents includes rodentproofing of buildings. The following precautions can be applied to reduce the probability of infection: • Water obtained from lakes or ponds on which waterfowl accumulate must be filtered and treated with chlorine to a level of 2 ppm. 4. salmonellosis. elimination of nesting places. and livestock. Some products kill within 1 hour. Caution in the use of rodenticides is required. Most single-dose compounds are toxic to nontarget animals and should be kept out of reach of children. Chemical methods to control rodents include bait and tracking powder. Bait has to be available continuously. Only extreme situations call for the use of a single-dose rodenticide with high toxicity. duck viral enteritis. bait should be available in both feed and water. poultry.or multiple-dose application. in powder mixed with grain. in the routes between the nesting site and the common food source. and other feed sources must be removed. appropriate management and sanitation. livestock. Multiple-dose compounds have a cumulative effect and will kill rodents after several feedings. Bait should be offered at stations located in the activity zone of rodents.
29
. These include Newcastle disease. and pasteurellosis. chlamydiosis. and shelter is an important part of a rodent-control program.

A commercial product. farms and processing plants. Chlorine can be added to drinking water at a level of 2 ppm using either sodium hypochloride or a gas chlorine installation. Standards for mineral and microbiological quality are shown in Table 4. This includes netting over air inlets. intestinal function and detract from optimal growth and feed conversion efficiency. and screen doors. For effective treatment the pH of water should be adjusted within the range of 6. 4.1.10-anthraquinone) can be applied as a paint suspension to roof areas.
30
. Water lines can be flushed and decontaminated with solutions as indicated in Table 4. which induces an irritation of the crop as a result of ingestion of minute quantities following preening.5 to 7. gantries and structures where resident pigeons and sparrows congregate. resident populations of potential reservoirs of infection are displaced from critical areas in feed mills. Microbiological contamination including fecal coliforms and viable Newcastle disease and avian influenza viruses can result in infection of flocks. Avipel® (9.• Buildings housing flocks and warehouses should be bird-proofed.2.5.7 Quality of Water Water supply for farms and hatcheries should be obtained from a municipal source which is filtered and chlorinated or from a deep (+50m) cased well or from a filtered and treated source from a dam or river.10-anthraquinone. exhaust openings. Since birds can differentiate between treated and non-treated surfaces by visualizing the UV spectrum of 9. Water containing mineral impurities can affect skeletal integrity. Avipel® will repel birds by a process of aversion to the compound.

32
.
Neglecting maintenance will result in rodent infestation.17.
Inadequate change room facilities may contribute to the introduction of infection to farms and hatcheries.
18.
19.
Backyard poultry and gamefowl serve as reservoirs for a wide range of infections which can impact the health and profitability of commercial poultry.

Accumulation of debris and discarded equipment encourages breeding of rodents.20. is cost efficient and consistent with accepted standards of biosecurity.
22.
33
.
Wet markets are a source of infection and special precautions should be taken to avoid introduction of disease onto farms by live bird traders.
Bulk delivery of grain reduces manual handling.
21.

23.
34
.
Manual handling of feed bags by workers may result in introduction of infection onto farms.

• Availability of specific vaccines.0 5. Circulating antibodies derived from the hen increase from day 1 to day 3 as yolk is absorbed. • Flock placement programs. If the initial vaccine is administered too early in relation to the decline in maternal
35
.2
Significance of Maternal Antibody in Relation to Flock Protection Maternal antibody (parental immunity) is stimulated in breeding stock in response to exposure to pathogens (naturally acquired maternal antibody transfer). High levels of maternal immunity often inactivate mild attenuated vaccine virus administered to chicks. • Risk of exposure. High maternal antibody is reflected in uniform and proportionally elevated antibody levels (titers) in progeny. or by vaccination (artificially acquired immunity). • Cost to benefit ratio associated with vaccination taking into account the risk of infection and financial loses from disease. A waning in titer occurs over the succeeding 1-3 weeks. according to a decay rate characteristic for the antibody. The dilemma facing poultry health professionals in developing vaccination programs for chicks is to specify the age of administration relative to the level of maternal immunity. IB and ND.5. • Intensity and consequences of adverse vaccine reaction.1
VACCINATION AND MEDICATION General Principles Vaccination involves the administration of a specific antigen to stimulate the immune system to produce homologous antibodies against viral. • Immune status of parent-level stock in relation to maternal antibody transfer. • Cost of acquisition and administration of vaccines.
5. and protozoal diseases. This interference phenomenon is important in timing the first “priming” dose of vaccine which stimulates immunity against IBD. Passively acquired maternal antibody may protect progeny against post-hatch exposure to certain pathogens for up to 2 weeks. Maternal antibodies (MABs) are transferred from the serum of the hen via the yolk to the chick. Vaccination programs should be based on the following considerations: • Diseases prevalent in the area of operation. Low and variable immunity in parent flocks is associated with early susceptibility of chicks. bacterial.

antibody. If the initial vaccination is delayed. the chick will not be protected.
Administration of mild IBD vaccine will be ineffective due to interference by high maternal antibody (mab) level. (Figure 5. field challenge of susceptible birds will occur.
C. At this age exposure to vvIBD will result in infection due to the ability of virulent field virus to overcome maternal antibody protection.
B. Flock will be susceptible to field IBD challenge at this time.1 RELATIONSHIP OF MATERNAL ANTIBODY AND VACCINATION
IBD Antibody Level
3000
waning of mab
2000
rise in titer following vaccination or challenge
1000
Antibody level corresponding to susceptibility to field IBD
0
A
7
B
14
C
21
Age Days
A.
36
. Administration of a mild IBD vaccine will stimulate immunity due to waning of maternal antibody.1)
FIGURE 5. Subsequent administration of intermediate IBD vaccine will reinforce immunity and raise circulating antibody level.

The principle of using a mild attenuated vaccine to establish immunity is emphasized.1 to 5. Table 5. For young breeder flocks. the risk and consequences of field infection. Administration of vaccines in drinking water or by spray are repeated successively during the growing period. routes. Although it is not possible to provide immunization protocols to suit specific circumstances.Other factors of importance in devising vaccination programs include the antigenicity (“strength”) of the vaccine virus. Various strategies have been adopted in the US and Europe to immunize broilers. Avian health professionals are advised to consult with local specialists and suppliers of vaccines to develop appropriate programs. breeders and pullets against exotic and catastrophic diseases including very virulent (vv) pathogenic IBD and vvND. Intensive vaccination programs are required to protect broilers. sequence. Table 5. The administration of oil emulsion vaccines to boost immunity is required to ensure satisfactory transfer of maternal IgM antibody to progeny. High uniform levels of maternal antibody are attained in breeders using attenuated live vaccines as “primers” followed by inactivated subcutaneous or intramuscular oil-emulsion “boosters” prior to onset of lay. the initial doses of vaccine may be delayed until 7-14 days of age to ensure active priming of the immune system. which are housed at high levels of biosecurity.3 illustrate practical programs which integrate vaccination against the diseases that occur commonly in Asia. Tables 5. and ages of administration.
37
.1 represents a comprehensive program to protect imported breeding stock from a wide range of diseases prevalent in an area of operation. Flock application at day old with attenuated IB/ND is followed by one or more “boosters” during growout.2 represents a comprehensive program to protect broilers in areas with both endemic vvND and vvIBD. Table 5. This program should only be considered as a general guide to the types of available vaccine. and environmental and management factors which may induce adverse vaccine reaction.3 represents a comprehensive program to protect commercial laying flocks against the usual range of diseases endemic in Asia.

5. • Post-hatch spray vaccination. Over-reliance on medication is both expensive and has negative flock and public health implications. using a manual or automatic syringe. in cabinets for mass-administration of aerosol vaccines to day old chicks. The actual administration of vaccines should be monitored by submission of serum specimens to a diagnostic laboratory for titer assay using ELISA or other acceptable technique. • Aerosol administration. • In ovo vaccination at 18 days of incubation using the patented Embrex InovoJect® system and alternatives. • Eye drop and intranasal routes. requiring handling of individual chicks. • Drinking water administration can be implemented at low cost but is of limited effectiveness against some infections. rearing stock and breeders. Medication should be used only after implementing accepted methods of prevention and control of disease. • Intramuscular injection.4
Medication Antibiotics and chemotherapeutic compounds are administered to flocks to treat outbreaks of disease. using a knapsack or electric sprayer to deliver vaccines to flocks as a coarse spray. • Wing-web stab to administer live vaccines by the percutaneous route directly to each bird. • Subcutaneous injection. to administer inactivated aqueous and emulsion vaccines to replacement pullets or mature stock.
38
.
5. The availability of drugs varies according to regulations in a specific country. including. The administration of drugs is generally a last resort to salvage the value of a flock and to reduce losses following infection. It is emphasized that appropriate control over the reconstitution of live vaccines is required to ensure potency. Important considerations which contribute to effective medication include: • The diagnosis should be established by isolation and identification of the pathogen by microbiological or other laboratory procedures.3
Administration of Vaccines Various methods of administering vaccines are used commercially. to administer either live or inactivated emulsion vaccines to chicks. are applied in hatcheries and during brooding of chicks.

biosecurity or vaccination exist. (Figure 5. breeding stock may be infected with a vertically transmitted disease. A schedule of therapeutic drugs and appropriate dose rates is depicted in Annex 41.• Pathogens should be shown to be susceptible to the selected drug using appropriate microbiological sensitivity assays. It is emphasized that if routine medication is required for successive flocks.
39
.2. • Response to medication should be monitored in relation to clinical improvement and. Alternatively. deficiencies in management. • Medication should only be initiated in anticipation of a positive benefit to cost ratio projection based on previous clinical response and a projection of losses. where possible. other livestock and consumers. • Medication should be administered in accordance with the manufacturer’s dose recommendations and for the suggested duration of treatment. Frequent or continuous administration of medication will result in emergence of drug resistant pathogens which will affect poultry.
Hatchery vaccination using an automatic injector.2) • Statutory withdrawal periods should be followed before the sale of live birds or processing to prevent drug residues in food products. by assay of compounds in feed or water.
24.

requiring service by non-farm personnel must be located adjacent to the perimeter fence.1
6. • Entry of personnel into each single-age flock should be through a shower module and require a complete change of clothing. spraying. electric and water meters and stand-by plants.3 m to exclude burrowing wildlife and should be topped with barbed wire to prevent unauthorized entry. at the grandparent or parent level in the country of operation may lead to infection of breeding flocks. • A 1 m wide strip on either side of the fence must be mowed so that any rodent or vermin activity can be detected. • A 3 m wide area around building perimeters must be kept free of all vegetation other than mowed grass to inhibit rodent and wildlife activity. • All equipment. • Small tools and equipment for mowing. Deficiencies in biosecurity. • All openings in the perimeter fence must be secured. resulting in suboptimal production and transmission of disease to progeny. Design features should include:
46
. mycoplasmosis. • No vehicles or equipment should be allowed within the farm area from the time of delivery of flock until depletion. such as feed bins. Rigid separation of the potentially “contaminated-outside” and the inner high security bird area should be maintained. The facility must meet the following requirements: • Perimeter of the site must be surrounded by a chain-link fence buried to a depth of 0.0
SPECIAL PROCEDURES RELATING TO CONTROL OF DISEASES IN POULTRY OPERATIONS Control of Disease in Multiplier Breeder Farms Suppliers of breeding stock in the USA and Europe maintain flocks free from salmonellosis.1.6. • Buildings housing flocks must be constructed to allow complete decontamination after depletion of flocks.1 Structural Biosecurity Multiplier breeder farms should be at least 3 km from any commercial or backyard poultry. and weighing must remain inside the fence during the life of the flock. and many other vertically transmitted diseases including specific retroviruses. gas tanks. Breeder farms should be operated on an all-in-all-out basis preferably with absolute separation of rearing and laying flocks.
6. vaccination.

6.2 Control of Disease on Commercial Broiler Farms
6. showering of personnel. should be constructed of concrete blocks. Movement of workers and crews among farms should be limited during each working day.
47
. such as ramps. 6.2 Operational Biosecurity Disease-surveillance procedures must be followed for all consumables used or introduced onto the site. 70 cm high.2. • All openings into the building should be screened to prevent access of free-flying birds. Moving flocks between farms can potentially expose birds to disease. Complete decontamination of equipment. and bacteriological cultures should be performed to monitor the effectiveness of decontamination. and provision of clean. Split-cycle rearing and laying is recommended. movement must proceed from the youngest to the oldest flocks to limit cross-transmission of pathogens. and consignments of feed should be assayed monthly for bacterial and fungal pathogens. site-clothing should be followed. such as a farm or hatchery each day. Metal personnel doors and installation of wire mesh screens over windows are recommended. including ceilings and side walls should be cladded with an impervious material such as galvanized steel or aluminum that can be easily cleaned and disinfected. must be thoroughly cleaned and disinfected after use. All equipment.1 Structural Biosecurity The general considerations relating to construction of houses as outlined for breeding facilities should be followed. Feed ingredients. This requires examination of each load of floor and nest litter for insects or foreign material. All equipment should be visually inspected. • Concrete floors should be smooth-troweled and sloped to lateral drains. This system has disadvantages relating to capital cost and management. If a production unit has birds of more than one age. supervisors or managers should visit only one production facility. • The interior surfaces of the building. nets. coops and vehicles.• Perimeter walls. and other wildlife.1. Ideally. Some integrators operate placement programs which house flocks from day old until the end of the egg-production cycle. rodents.

The installation of bins (silos) for bulk-delivery of feed is strongly recommended to reduce the risk of introduction of disease associated with manual handling of feed bags.6. Appropriate programs of disease detection and vaccination should be implemented. The intensity of disease prevention measures depends on the risks and consequences of infection.2. It is necessary to transport broilers intended for sale to a remote site for selection and purchase by dealers.
48
. This approach to live bird sales allows complete depopulation of farms with realistic interflock intervals of at least 10 days. These are adapted from the general biosecurity recommendations and the management guidelines issued by breeders.2 Operational Biosecurity It is impossible to maintain adequate biosecurity when live birds are marketed directly from growing farms.

S.
32. (Courtesy of Ross Breeder Inc.
Isolated breeder farm in a rural U.30.
49
.)
31.
Maintaining multi-age farms or establishing units in close proximity creates problems relating to control and eradication of chronic diseases such as mycoplasmosis and coryza.
Well-ventilated convection house using indigenous materials suitable for broiler growing. location remote from nearest public road. Materials used for construction are incompatible with disinfection. The entire farm is surrounded by secure fencing and a high level of biosecurity is imposed to prevent introduction of disease which could be spread vertically to progeny.

Litter beetles (Alphitobius diaperinus) serve as reservoirs of Marek’s disease virus. Processing plant has a throughput of 100.. Salmonella spp..
34.
Installation of mechanical washer to decontaminate coops before return to farms. and other infectious agents. Pasteurella spp.33.
35.
Delivery vehicles should be disinfected before entry to farms to avoid introduction of pathogens.000 birds/week.
50
.

• Routine disease monitoring is necessary. Procedures include postmortem examination of dead birds when mortality exceeds standard levels and periodic serum antibody assays to determine the immune status of flocks. Laborers invariably have contact with backyard chickens which are reservoirs of disease. salmonellosis or laryngotracheitis. which can be decontaminated at the point of entry to the farm. especially when products are distributed through dealers.1 Operational Biosecurity • It is suggested that small-scale egg-production units in Asia should be operated on an all-in-all-out basis with separate rearing and laying units. Culled hens should be transferred from the production unit to a remote site for sale to live-bird dealers. If this is not possible. • Appropriate vaccination programs should be implemented to protect flocks against challenge. Change-room and shower facilities are required and protective clothing should be provided to prevent introduction of disease onto farms by workers. pasteurellosis and Marek’s disease.
51
. it is recommended that appropriate biosecurity procedures should be implemented. • Since rodents are reservoirs of salmonellosis.3. and where possible. effective programs to suppress vermin should be an integral component of a disease prevention program. pullets should be obtained from a source known to be free of vertically transmitted infections or diseases characterized by a permanent carrier state such as coryza.3
Control of Disease in Commercial Egg Production Units
6.6. bulk-delivered feed is recommended to obviate manual handling and delivery in bags. • Care should be exercised in using recycled egg packing material. Plastic flats should be used. Movement of personnel should be controlled. relatively large numbers of laborers are employed to feed flocks and collect eggs. • Due to the low level of mechanization in laying units in Asia. Exposure to disease will lower egg production and reduce quality following transfer to laying units. In view of the high investment in facilities and flocks.

52
.36.
Simple single-tier layer cage installed in open-sided house incorporating manual feeding and a trough drinker. These inexpensive systems are extensively used in Asia.
38.
The undeveloped comb of a culled pullet.
Well developed comb of a healthy 25 week old Leghorn hybrid hen.
37. but labor input is high and the system is associated with problems of manure disposal and houseflies.

4
Control of Disease in Hatcheries
6. • All vehicles should be disinfected before entering a hatchery. and metal boxes should be thoroughly dried after disinfection. Door seals should prevent crosscontamination by air movement. processing. To prevent mold growth. To prevent movement of air from “dirty” to “clean” areas. Facilities should be provided to disinfect all entering vehicles. • Hatcheries should be designed with a floor plan. 6. • An appropriate cleaning and disinfection program should be followed. disposal of waste. these should not be reused. Hatchery design should allow for future expansion and incorporate provision for drainage. The facility should be supplied with chlorinated water. • Air intakes should never draw air from the vicinity of an exhaust duct.
53
.2 Operational Biosecurity • A dedicated egg-collection vehicle should be used for fertile eggs. in accordance with the recommendations of suppliers of chemicals and equipment. and chick dispatch area. • Installations should be capable of adequately cleaning and disinfecting all setter and hatching trays. trays. One central point of entry adjacent to the change room should be designated. washing of chick boxes and trays. cold room for eggs. shower.4. and change room facilities for staff and visitors should be available and used routinely. and all entrances to the building should be located inside the fenced area. Egg-delivery vehicles should be decontaminated and fumigated daily. ventilation system and interior finishes conforming to accepted standards of hygiene. Potentially contaminated areas are the chick takeoff. which are graded and decontaminated by spray or fumigation on the breeder site. Since fiber trays and cardboard boxes cannot be cleaned and disinfected.1 Structural Biosecurity • Access to the hatchery and any associated buildings should be restricted. and egg flats used in the hatchery. positive pressure should be maintained in egg setter bays. recording date and time and the previous farm or site visited. and washing areas. all egg flats.4. plastic egg flats and packaging material should be color-coded to the farm of origin.6. The facility should have a secure fence. • Adequate laundry. A log book should be kept for entry of visitors or deliveries to the hatchery. chick boxes. Work flow should permit separation of potentially contaminated and “clean” areas. Where possible. • Reusable plastic egg trays can be used to collect commercial broiler eggs but should be cleaned and disinfected after each use.

Setter racks should be cleaned and inspected before return to the breeding farm. • Chick-delivery vehicles should be decontaminated daily. Vaccination equipment should receive special attention according to manufacturers’ recommendations. vehicles. Chick boxes should be cleaned on return to the hatchery. setters rooms. hatchability. and the method and frequency of application. and surface swabs. centrifugal air sampling. hatcher rooms. Routine tests should include incoming eggs. Broken eggs should be removed from setters daily. Procedures should specify disinfectants. concentration. the chick-processing room should be cleaned and disinfected. • Hatchers and hatching equipment should be cleaned and disinfected after each take-off. Routine fogging or fumigation is necessary to prevent aspergillosis. • Quality control procedures include examination of hatchery fluff. setters. chick-processing rooms. exposure of media plates to air. agar gel impression disks. Setter rooms should be disinfected daily under supervision and inspected to ensure compliance with standard procedures. and chick livability should guide the choice of disinfectants and dilution rates. with appropriate action to prevent cross-contamination.• Single-stage setters should be cleaned and disinfected after each transfer. • The hatchery sanitation program should be incorporated into a hatchery manual. Correlations between the microbiological test results.
54
. • Routine monitoring of cleaning and disinfection should be carried out and appropriate remedial action should be taken if the prevalence of omphalitis or aspergillosis results in a 0. including all work surfaces and installations. • At the end of each hatching day. Procedures should be reviewed and updated as necessary. Only properly trained personnel should clean and apply disinfectants. hatchers after disinfection. the egg room. exhaust ducts. and the water supply.5% increase in first week mortality.

Setter bay in small hatchery showing high standards of surface finishes consistent with acceptable hygiene and decontamination.
55
.39.

4 Fats Suboptimal levels of essential fatty acids including linoleic and linolenic acid will depress egg size in high-producing hens.
Under commercial conditions multiple deficiencies often occur and signs and lesions associated with suboptimal intake of a specific nutrient may not be clearly defined. A deficiency in lysine may occur in wheat and maize-based diets and will result in depressed growth rate and feed conversion efficiency in broilers. essential fatty acid deficiency will result in
57
.2. feed conversion efficiency. mature birds will lose weight and hens will show a decline in both egg size and egg numbers. 7.2.• • • •
be sub-optimal. 7.2 Low Energy Intake Most poultry will compensate for low energy density by consuming a greater quantity of feed. Male breeders will become infertile. The effect of restricting energy intake will be exacerbated by low environmental temperature or improper management of brooding and ventilation systems during the early growth phase. both egg size and egg numbers will be reduced. Growth rate of immature stock will be depressed. Under conditions of feed restriction or extreme competition. In the case of mature flocks. Flocks deprived of energy will show increased susceptibility to infection. The nutrient quality of ingredients may be depressed by excess moisture. immune response and reproductive efficiency. 7. mold contamination or inappropriate processing. Destruction of nutrients can occur in feed due to oxidation. Deficiencies in energy and essential amino acids will exacerbate the effects of viral malabsorption syndrome and intestinal damage caused by coccidiosis or endoparasites. Deficiencies may occur due to deletion of specified ingredients or supplements from rations. Chemical antagonists in feed may increase the nutritional requirements of nutrients. It is emphasized that suboptimal levels of essential amino acids will not result in any specific clinical sign or lesion other than a failure to attain accepted production standards.3 Deficiencies of Proteins or Amino Acids Low protein intake will depress growth rate. Methionine deficiency in diets containing maize and soybean meal will result in a low growth rate. Under conditions of elevated temperature.2.

prolonged storage of diets. and the presence of metal catalysts in storage tanks. Ingredients containing high levels of saturated fatty acids are susceptible to this process which yields toxic peroxide free radicals which damage cell membranes and overwhelm the inherent biological antioxidant systems at the cellular level. • Avitaminosis A Chicks will show poor growth and feathering and in advanced cases. Most commercial antioxidant additives for feed use contain ethoxyquin. sodium bicarbonate as a buffer in a hydrated aluminum silicate carrier.degeneration of the liver and possibly rupture of the capsule. with hemorrhage into the body cavity. Fertility and hatchability of breeders will be adversely affected. These compounds are combined with a chelator such as citric acid. Autoxidation is prevented by supplements which chelate metallic ions and scavenge and inactivate free radicals. The significant deficiencies encountered in commercial poultry production include. vegetable oils and animal tallow will allow oxidative rancidity to occur. Since vitamin A is concerned with the integrity of respiratory and gastrointestinal mucosa.6 Vitamin Deficiencies Deficiencies of vitamins may occur following inappropriate formulation. carcass meal. (Fatty liver syndrome) 7. ataxia (inability to stand). Antioxidants can also be added to specific ingredients such as fishmeal or animal byproduct meal in liquid form during manufacture. flocks subjected to avitaminosis A will show a high prevalence of E. 7. and/or butylated hydroxy toluene.2. coli and other bacterial infections and will be more severely affected by endoparasites and coccidiosis. xerophthalmia (“dry eye”) and chronic purulent conjunctivitis (accumulation of yellow caseous material beneath the eyelids). the use of impotent commercial preparations or destruction of nutrients in feed by oxidation. rice bran.5 Oxidative Rancidity Failure to stabilize ingredients such as fishmeal. The initiation of oxidative rancidity characterized by free radical formation is stimulated by high ambient temperature. Laying hens subjected to avitaminosis A will show a deterioration in internal egg quality and a high prevalence of blood spots. Addition rates to diets at levels equivalent to 125 ppm ethoxyquin are suggested.
58
.2. Antioxidant products are required for ingredients containing in excess of 10% fat.

Affected birds aged 4 to 7 weeks show a disinclination to walk. Vitamin D3 deficiency results in gross enlargement of the parathyroid glands.Diagnosis of avitaminosis A can be confirmed by microscopic examination of the trachea and oral mucosa. • Vitamin E Deficiency Vitamin E is required in complex biochemical functions. Swelling of the joints is noted together with depressed growth rate and poor feathering. Transudative diathesis occurs in chicks fed diets deficient in vitamin E or containing free radicals. Rickets can be confirmed by histological examination of the proximal end plate of the tibia and parathyroid gland tissue. In mature laying and breeding stock. The presence of free radicals will result in destruction of vitamin E both in the feed and in vivo.1 to 0. (0. Transudative diathesis can be partly reversed by supplementation of diets with adequate quantities of selenium. Affected flocks show a gradual decrease in egg production and a marked deterioration in shell quality. a deficiency of vitamin D3 results in osteomalacia characterized by decreased skeletal density.3 ppm). Both immature and adult flocks will show kidney degeneration and the accumulation of urate in the ureters. • Vitamin D3 (Cholecalciferol) Deficiency A deficiency in vitamin D3 will lead to rickets in immature flocks. Three specific conditions occur in young chickens. Ascending mortality is associated with paresis and paralysis in caged hens which are unable to stand to feed and drink. in which normal columnar epithelial cells regress to multiple layers of flattened cells. In advanced cases urate deposit on the viscera (visceral gout) is observed at postmortem examination. costochondral (rib to spine) junctions are enlarged and the end plates of the long bones are irregular due to defective mineral deposition required for osteogenesis (bone formation). Transudative diathesis results from degeneration of the endothelium (lining of the blood vessels) resulting in leakage of plasma into surrounding tissues. On post-mortem examination decreased skeletal density is evident. Encephalomalacia occurs in chicks fed diets in which vitamin E has been destroyed by oxidative rancidity. The characteristic change comprises squamous metaplasia. preferably in the organic
59
.

The condition can be diagnosed by determining the prothrombin time which is delayed from a normal 20 . thiamine and pyridoxine deficiencies.(selenomethionine) form which is more available than inorganic sodium selenite. On post-mortem examination sub-serosal hemorrhage is evident. incoordination. and terminal recumbency with cycling motions of the legs. The differential diagnosis of ataxia in chicks includes avitaminosis A. Recently. arenavirus infection has emerged which leads to hypoglycemia which results in recumbency and tremors. Encephalomalacia is the most commonly encountered condition associated with avitaminosis E due to a deficiency or in vitro destruction in tropical countries. avian encephalomyelitis (epidemic tremor).20 days of age and may result in the death of up to 10% of the flock. Muscular Dystrophy occurs in the skeletal muscles. Subcutaneous hemorrhages are noted on the head and beneath the wings of affected birds. and anticoagulant rodenticide toxicity. • Vitamin K Deficiency This condition occurs in caged flocks fed rations deficient in vitamin K. the ventriculus (gizzard) and myocardium (heart muscle). mycotoxicoses. Onset is at approximately 10 . The effect of avitaminosis E is exacerbated by concurrent deficiency of sulphur-containing amino acids and selenium. Affected birds do not recover. Organophosphate toxicity which causes incoordination and death preceded by convulsions is usually peracute in onset and involves the entire flock.
60
. The characteristic lesion comprises punctate hemorrhages within the cerebellum and occasionally the cerebrum. The condition can be confirmed by histological examination of brain tissue from affected birds.30 seconds to values exceeding 5 minutes. Flocks showing nutritional encephalomalacia will respond to administration of water dispersable vitamin E and stabilization of diets with antioxidants and supplementary vitamin E. Malacia (softening) of the brain is evident. Differential diagnoses for vitamin K deficiency include hemorrhagic syndrome. Infected birds demonstrate ataxia.

30 days. Histological examination of the major peripheral nerve tracts will show myelin degeneration. bone ash determinations. amprolium. These avitaminoses are seldom diagnosed as single entities in commercial poultry in tropical countries but contribute to a general pattern of poor growth and depressed reproductive efficiency in mature flocks. Calcium and phosphate deficiencies may be diagnosed by histological examination of bones and the parathyroid gland. These changes also occur with pantothenic acid deficiency and reoviral malabsorbtion syndrome. niacin. Chicks from deficient flocks have abnormal development of down feathers. Affected flocks will demonstrate low growth rate and poor feathering. There are no macroscopic lesions associated with thiamine deficiency. The principal sign comprises dermatitis of the feet and of the skin adjacent to the angle of the beak. pyridoxine and folic acid can be reproduced under experimental conditions. In
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. • Calcium and Phosphorus Deficiency In immature flocks a deficiency of either calcium or available phosphorus or an imbalance in these nutrients will result in rickets. and is referred to as “club foot” or “curled toe paralysis”. to diets. hatchability is lowered and embryonic malformations of the feet are noted.• Vitamin B1 (Thiamine) Deficiency Avitaminosis occurs as a result of failure to add thiamine to vitamin premixes or occasionally as a result of excessive addition of the anticoccidial. osteomalacia may occur. The principal sign of thiamine deficiency in 10 to 20 day old chicks comprises incoordination and an abnormal retraction of the head (“star gazing”). In laying hens and breeders. • Vitamin B2 (Riboflavin) Deficiency This condition is characterized by rotation of the legs in chicks aged 10 . • Biotin Deficiency Affected flocks demonstrate poor growth and feathering and elevated mortality. and analyses of representative feed samples. Breeding flocks fed diets deficient in riboflavin show low egg production and hatchability. • Other Vitamin Deficiencies Deficiencies of pantothenic acid. In breeding flocks. • Manganese Deficiency Manganese deficiency leads to chondrodystrophy which results in deformation of the distal tibiotarsus and proximal tarsometatarsus.

• Sodium and or Chloride Deficiency Failure to add supplementary salt to poultry diets composed of maize and soybean meal will result in depressed growth rate and decreased egg production. The quality of soybean meal incorporated into poultry diets is an important contributor to performance of broilers and mature stock.
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. • improved market share and profitability. • improving client and in-company acceptance of feeds. 7.3 Quality Control in Feed Manufacture It is necessary to implement a comprehensive quality control program to monitor the nutritional value and composition of ingredients and to ensure thorough mixing and correct identification of diets.extreme cases displacement of the gastrocnemius tendon occurs as perosis (“slipped tendon”). normal values. Young chicks will show tail picking and cannibalism. Routine assays should include: • moisture • crude protein • fat • urease activity • protein solubility in 0. • Zinc Deficiency Deletion of zinc from the mineral premix will result in decreased growth rate and chondrodystrophy. The direct and indirect benefits of comprehensive quality control invariably outweigh the capital and operating costs involved.02% potassium hydroxide Information on analytical procedures. Standard operating procedures consistent with industry practice should be developed and a quality control program implemented based on laboratory analysis and a review of production records. A commitment to the principle of total quality management generates the following benefits: • enhanced performance of flocks by obviating toxicity and deficiency in diets. storage of soybean meal and formulation is available from an ASA International Office.

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.
41.
Quality control is an important component of feed production and requires trained technicians and suitable equipment.
Purulent conjunctivitis due to Avitaminosis A.40.

43. decreased mineralization of the mandible and maxilla allows extensive lateral movement of the beak.
The long bones of chicks with rickets can be bent without fracture.42.
Avitaminosis A characterized by nodular lesions in the mucosa of the esophagus.
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. In this case.
44.
Chicks affected with rickets show lowered skeletal density.

46.
Installation of a large capacity black-painted metal storage tank for feedgrade blended oil in a tropical area will lead to rancidity with consequential destruction of fat-soluble vitamins.
47.
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. Horizontal orientation increases surface area and oxidation.
Broiler chicks aged approximately 14 days showing lateral recumbency associated with nutritional encephalomalacia.
Hemorrhage within the cerebellum characteristic of nutritional encephalomalacia due to a deficiency of Vitamin E or destruction of this nutrient by free radicals in oil undergoing rancidity.45.

48.
Chicks showing edema of the intermandibular region due to transudative diathesis.
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.
49.
Hemorrhage and transudate beneath the wing associated with transudative diathesis due to destruction of Vitamin E following oxidative rancidity.
Subcutaneous hemorrhage beneath the wing of a cagehoused pullet due to Vitamin K deficiency.
50.

This condition can be prevented by lowering the energy value of the feed and ensuring that sulphurcontaining amino acids and choline are at an appropriate dietary inclusion rate.
53.51.
Fatty liver syndrome in a mature hen results in rupture and hemorrhage into the body cavity. Measures to reduce heat stress are required to minimize losses.
52.
Hyperkeratosis (thickening of the skin) of the plantar surface of the feet associated with pantothenic acid or biotin deficiency.
Hen showing sternal recumbency due to osteomalacia.
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.

4
8. Marek’s disease virus is responsible for neural and visceral tumors. The virus is resistant to environmental exposure and can remain viable for long periods in houses especially if units are not decontaminated between cycles.8. proventriculus. Marek’s disease virus is immunosuppressive and infected broiler and pullet replacement flocks are susceptible to a wide range of viral and bacterial infections. and Europe. Infected birds shed “dander” (feather dust) contaminated with virus which can be distributed by wind. Occasionally visceral lesions are observed and the kidney.3
Transmission Exposure to MDV occurs by horizontal infection. Clinical Signs Involvement of the peripheral nerves results in paresis (weakness) of the legs or wings which progresses to paralysis. Pathology Enlargement of the feather follicles is observed on the skin of de-feathered broilers and results in condemnation of carcasses in the USA. equipment.6
Diagnosis and Confirmation The gross appearance of neural lesions is generally diagnostic.5
8.
8. Canada. eye.
8. erosive losses of up to 20% occur in non-protected or inadequately vaccinated flocks. Exposed broilers show increased mortality and condemnation rates at processing. The characteristic MD lesion comprises enlargement of the peripheral nerves of the sciatic or brachial plexus.0 8.1
MAREK’S DISEASE Etiology An oncogenic (tumor-inducing) herpesvirus Occurrence and Economic Significance Marek’s disease affects commercial chicken flocks from approximately 5 to 35 weeks of age in all areas of the world.2
8. Death occurs in both caged and floor-housed birds as a result of dehydration and persecution. non-immunized flocks up to 60 weeks of age. Generally. Highly pathogenic (vvMD) strains of the virus are responsible for acute outbreaks of mortality which may attain 50% in exposed. and personnel. ovary or other organs may be affected. Histological examination of nerve and visceral lesions will show characteristic
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.

7 Prevention Vaccination of broiler embryos using in ovo administration on the 18th day of incubation or by subcutaneous administration of vaccine to broiler. 8.g. Three types of vaccine are available: Type 1: attenuated chicken strain (e.g.g. Improper vaccination technique may lead to defective immunization with resulting “breaks”. The causal virus may be isolated and identified by submitting tissues to a suitably equipped laboratory using specific tissue culture techniques. allowing commercial progeny to be immunized using the less expensive HVT strain alone or in combination with the potentiating SB1 strain. Cell-associated.lymphocytic proliferation. HVT) Due to the interfering effect of maternal antibody on HVT it is advisable to alternate vaccine types in successive generations. frozen vaccines require special storage in a liquid nitrogen canister. SB1) Type 3: apathogenic turkey. parents should be vaccinated with Rispen’s strain. breeder or replacement egg-strain chicks at day old. an emerging condition of unknown etiology. but suspected to be an autoimmune response to vaccination in specific strains of commercial laying hens. It is essential to place day old chicks in houses which have been thoroughly decontaminated to allow vaccinated flocks to develop immunity. Rispen’s) Type 2: apathogenic chicken strain (e. In countries where highly pathogenic MDV occurs. The condition should be differentiated from botulism and from “transient paralysis”. Rearing farms and broiler growing units should be operated as single-age units with all-in-all-out cycles.
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. strain (e. Careful reconstitution using the diluents supplied by the vaccine manufacturer is necessary to maintain viability of the vaccine virus.

Infectious Bursal Disease is a major restraint to productivity and profitability in the poultry industries of both industrialized and developing nations. Pathogenic Delaware variants A through E predominate in the USA and Central America. non-pelleted feed containing inadequately heattreated poultry by-product meal.1
Type 2: 9.4
.
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9. Indirect infection with IBDV occurs within days of placing chicks as the agent can survive in a contaminated environment for up to 3 months. ruffled plumage and white diarrhea.2
Occurrence and Economic Significance The disease affects immature chickens world wide. Asia and Africa. and clothing of personnel are frequently sources of infection.9. depending upon the pathogenicity of the IBDV strain and the susceptibility of the flock.0
INFECTIOUS BURSAL DISEASE synonyms IBD:Gumboro Disease Etiology Type 1 avibirnavirus strains Type 1: Both classic and highly pathogenic (vvIBD) serotypes are recognized. There are no characteristic signs specific to IBD.
9. Affected birds are depressed and show recumbency. housing. Acute infection with classic mild or variant strains results in up to 5% mortality. The vvIBD strains occur frequently in the Middle East. The variants are more immunosuppressive than the classic strains. Contaminated equipment. Avibirnaviruses are immunosuppressive and predispose flocks to intercurrent viral pathogens and secondary bacterial infection.3
Transmission Direct contact of young birds with infected flocks in multi-age units results in persistent “rolling” infection which is difficult to control.
9. Very virulent (vvIBD) virus may kill up to 50% of susceptible flocks. Clinical Signs Flocks are affected acutely and show variable morbidity (5-50%) and rapidly ascending mortality (5-50%). Turkey strains are apathogenic to chickens.

This is required if chicks are exposed to IBDV at the time of placement. This program will promote transfer of high and uniform levels of antibodies to progeny. coli septicemia are frequent complications following exposure to respiratory viruses especially with superimposed climatic or environmental stress. mild strain vaccines may be administered from dayold to 14 days. Recovered birds show bursal atrophy. Subsequent administration of intermediate strain vaccine may be necessary depending on factors including: • Risk of infection. A combination of live IBD virus with corresponding antibody (Bursaplex®) is available to be administered either in ovo or at day-old by the subcutaneous route.
9. Diagnosis Acute bursal changes are generally diagnostic. In North America a mild live multivalent (classic and variant) vaccine is administered by the in ovo route to provide initial stimulation of the immune system. • Strains of virus prevalent in the area of operation. can identify specific IBDV isolates. Sectioning the organ may show hemorrhages. In areas of the world where relatively avirulent strains of IBD virus occur. This vaccine is effective in the presence of high levels of maternal antibody. Broiler and replacement layer chicks should be vaccinated with live-attenuated vaccine which primes the immune system.9. IBDV can be isolated in specific pathogen free embryonated eggs or on tissue culture. Histological examination of bursas from broilers or pullets at various stages of the disease will show edema progressing to atrophy. Airsacculitis and E. In acute cases the characteristic lesion comprises enlargement of the bursa of Fabricius which is often surrounded by gelatinous exudate. Antibody response in vaccinated flocks should be routinely monitored using ELISA serology.6
9.
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. • Intercurrent exposure to respiratory viral infections.5
Pathology Dehydration and muscular hemorrhages are evident in dead birds.7
Prevention Parent flocks should be immunized with one or more attenuated live (mild or intermediate) vaccines followed by an oil-emulsion booster. Serotyping carried out in reference laboratories using monoclonal antibodies.

This formula relates the initial antibody level to the rate of decline in maternal antibody to obtain the optimal age for vaccination.D.The age of administration of live attenuated vaccines depends on the level of maternal antibody and the risk of infection. (Courtesy of Dr.82 is the mean half life (in days) of maternal antibody. Age of vaccination: ELISA titre . P.36 / 2.
56. Selection of the age of vaccination is determined by applying the following formula based on the results of ELISA serology at day old. Lukert.22. (the threshold of protection) and 2. AAAP Slide Set)
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. It is necessary to maintain strict levels of biosecurity and to operate flocks on an all-in-all-out basis in areas where severe infectious bursal disease is endemic. In areas of the world where the very virulent (vvIBD) strain occurs. intermediate-plus (“hot”) vaccines are administered in drinking water.36 is the square root of 500 ELISA units.82 (+1) days
where 22.
Acute infectious bursal disease showing chicken with copious white diarrhea.

The virus causes stunting and increased susceptibility to secondary viral and bacterial infections including dermatitis which results in downgrading. Contaminated live vaccines prepared from infected embryos are thought to have been responsible for widespread dissemination of CA infection prior to recognition of the virus.7 Prevention Immunization of breeder flocks during the age period 12-15 weeks using an attenuated vaccine. with onset at 10 days. Primary CA mortality occurs during the age period 15-20 days. following secondary bacterial infection.4 Clinical Signs Morbidity is variable. Gangrenous dermatitis of the extremities (“blue wing”) is noted.3 Transmission Both vertical and horizontal routes of infection occur under commercial conditions. 10. Septicemia and gangrenous dermatitis occur in older birds. The PCR (polymerase chain reaction) assay can identify CAV T-cell and B-cell lymphoblastoid cell line tissue cultures can be used to isolate the agent in suitably equipped laboratories. MDV and reticuloendotheliosis virus (REV) (a retrovirus).2 Occurrence and Economic Significance The infection is widespread in broiler and replacement parent and layingstrain pullets. Chicken infectious anemia virus (CAV) is immunosuppressive and is responsible for mortality of up to 10% in affected broiler flocks. 10.1 Etiology A non-enveloped icosohedral DNA-virus. Affected chicks are pale and stunted.0 CHICKEN ANEMIA 10. 10. Marked anemia may be observed with corresponding hematocrit values below 15%. classified as a circovirus.5 Pathology Thymus and bone marrow atrophy and muscular hemorrhages are characteristic.6 Diagnosis ELISA and VN serology can confirm infection of flocks. 10. 10. The pathogen is synergistic with IBDV.10. 10.
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. Either vaccination or natural exposure will confer immunity to progeny through maternal antibody transfer.

subcutaneous hemorrhage. Control of respiratory infections and other immunosuppressive agents is essential to reduce the impact of CA. and transudate due to chick anemia virus.
60.
Pale bone marrow indicating immunosuppression associated with chick anemia virus or mycotoxicosis.
Wing of 14-day old broiler showing edema. Appropriate management procedures can reduce the effects of primary CA infection.
61.
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.Biosecurity procedures are required to prevent horizontal infection.

The severity and financial impact depends on climatic and management stress and intercurrent exposure to pathogenic E. Velogenic and mesogenic forms are exotic to the USA. moderately lethal disease with nervous and respiratory signs.3 Transmission ND virus is highly contagious.0 NEWCASTLE DISEASE 11. Canada.
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. highly lethal disease. Severe losses from mortality. • Mesogenic virus causes acute. the UK and other European countries but are widespread in Asia. The cost and consequences (respiratory stress) of vaccination are significant.11. • Lentogenic virus is responsible for mild respiratory infection. 11. • Velogenic-viscerotropic virus (vvND) infection results in acute onset. especially during winter and following immunosuppression.2 Occurrence and Economic Significance Three categories of viral pathogenicity result in different clinical forms of the disease. coli and other viral respiratory disease and immunosuppressive agents. • Companion birds. Disruption of trade and the cost of eradication of vvND in non-endemic countries imposes a significant burden on producers and the public sector after outbreaks. Infection occurs either by the inhalation of virus in aerosol form or ingestion of contaminated feed or litter. Africa. • Wind dispersal may occur over distances of 5 km. backyard flocks and gamefowl serve as reservoirs. and Latin America. • Direct and indirect contact with contaminated material (fomites) is associated with deficiencies in biosecurity. The lentogenic form is responsible for erosive losses in broilers including lowered gain and feed conversion efficiency and elevated mortality and condemnation.1 Etiology Antigenically related strains of Avian paramyxovirus. The lentogenic form is encountered in most poultry-producing areas including the USA. depressed egg production and lowered feed conversion efficiency occur as a result of exposure to vvND. 11. type 1.

Lentogenic Mild conjunctivitis and tracheitis are observed. Mild to inapparent respiratory signs are noted but negligible mortality occurs in uncomplicated cases. These changes are not specific to vvND and may be observed with highly pathogenic strains of avian influenza and vvIBD. 80% in 5 days) accompanied by respiratory and nervous signs.
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. Mesogenic Variable to high morbidity is evident in an exposed flock which will show moderate mortality characterized by nervous and respiratory signs. 50% in 3 days.11. Lentogenic ND may be responsible for asymptomatic drops in egg production in incompletely immunized commercial layer or breeder flocks. 11. coli. Lentogenic Acute onset with moderate to high morbidity. Recovered flocks show septicemia and airsacculitis due to secondary infection with E. Exposure of immunized flocks results in variable decline in production. 11. The virus can be detected applying PCR technology to obtain a provisional diagnosis within a working day.4 Clinical Signs Velogenic Viscerotropic Newcastle Disease This form is characterized by acute onset with up to 100% flock morbidity and rapidly ascending high mortality (20% in 2 days. Identification and characterization of the virus by a suitably equipped laboratory is the usual confirmatory procedure. In susceptible commercial egg production flocks and breeders. peracute cessation of production occurs with the presence of shell-less eggs due to premature oviposition.6 Diagnosis Isolation. An acute drop in egg production occurs in susceptible mature flocks with the presence of shell-less eggs. Severe tracheitis and pulmonary congestion are evident in acute cases.5 Pathology Velogenic Prominent hemorrhages occur throughout the digestive tract especially in the mucosa of the proventriculus and gut-associated lymphoid tissue.

An optional 45 week multivalent oil inactivated emulsion may be administered to boost maternal antibody transfer. • Recombinant pox and HVT-vector vaccines expressing the fusion (F) protein of NDV are available for either in ovo or subcutaneous vaccination. 11. • Administration of a preparation comprising live virus with complementary antibody (Newplex®) by the in ovo route at 18-days of incubation is protective in countries where the vaccine is available. hemagglutination inhibition and serumvirus neutralization) demonstrates the presence of antibodies which indicates exposure to ND virus and the titer (level) can differentiate between field infection and previous vaccination. risk of exposure. depending on antibody titer of the flock. Breeders may be immunized with mesogenic-strain vaccines in some countries. and economic factors. This expedient is only justified if birds have previously received one or more live attenuated lentogenic vaccines. Conventional programs: • Lentogenic infection of broilers can be prevented by day old administration of aerosol or eye drop vaccine using Hitchner B1 with subsequent boosters in drinking water or by the aerosol route.Retrospective serology (ELISA. A variety of vaccination programs can be followed depending on the risk of infection. • In areas with a defective cold-chain the V-strain live thermostable mutant ND can be distributed to subsistence and backyard flocks. followed by multivalent oil inactivated emulsion at 18-20 weeks. In countries with endemic vvND.7 Prevention Vaccination. by the aerosol or eye drop route. rigorous programs are implemented. virulence of agent.
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. Hitchner or LaSota vaccine is administered to broilers by the aerosol route at 10 day intervals thereafter. incorporating day-old subcutaneous emulsion vaccine together with attenuated live vaccine by the eye-drop route. • Subsequent vaccinations include 24 day. and 8 week Hitchner B1 or LaSota in non-chlorinated drinking water. • Lentogenic infection of breeders can be prevented by 10 day administration of Hitchner B1. and other factors relating to the operation. management system.

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. (Courtesy University of Pennsylvania)
64.62.
Broiler flock showing high morbidity and mortality due to velogenic Newcastle disease or HPAI.
Torticollis in an immature chicken infected with velogenic Newcastle disease.
63.
The trachea yields virus for PCR analysis and for isolation and identification of viral and bacterial pathogens of the respiratory tract.

Hemorrhage of the mucosa of the proventriculitis due to velogenic Newcastle disease. infectious bronchitis. (Courtesy of the University of Georgia). or mild avian influenza. coryza.
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.
66.
Acute onset of ocular discharge accompanied by high flock morbidity may denote infectious laryngotracheitis.65.

Proportionally more severe lesions occur with pathogenic virus strains which produce severe hemorrhagic tracheitis with the presence of blood clots.4 Clinical Signs The severity of LT is influenced by the strain of virus. immune status of the flock and environmental conditions. conjunctivitis and swollen heads.3 Transmission Direct contact with clinically affected chickens or recovered permanent carriers.1 Etiology Gallid herpesvirus 1. 12. or contaminated personnel or equipment.12. The fluorescent antibody technique may be used to demonstrate LT antigen in respiratory mucosa.5 Pathology Hyperemia of the tracheal mucosa is present in most cases. Mild LT results in lowered growth rate and feed conversion efficiency and elevated mortality and condemnation in broilers. 12. The LT virus can be isolated using SPF embryos or tissue culture with identification applying immunofluorescence or serum-virus
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. 12.6 Diagnosis Histopathology usually reveals the presence of intranuclear inclusion bodies in the epithelium (cell lining) of the trachea. Wind dispersal over 3 km has been documented.0 INFECTIOUS LARYNGOTRACHEITIS Synonyms LT & ILT 12. 12. In severe cases. Aggregations of desquamated epithelium and blood clots may obstruct the glottis resulting in asphyxiation. Indirect contact through dust-laden vehicles.2 Occurrence and Economic Significance Laryngotracheitis is distributed worldwide but is frequently regional in prevalence or seasonal in incidence. Mild to severe cases show acute onset with respiratory signs (snicking and gurgling). 12. Moderate to severe strains of LT result in proportionately higher morbidity and mortality in both mature and rearing stock with losses approaching 50% with concurrent environmental stress and other infections. Decreased egg production occurs following exposure of mature susceptible flocks. birds show expectoration of blood accompanied by cyanosis of the head due to dyspnoea.

New vaccine candidates based on recombinant DNA technology should overcome the problem of reversion associated with live modified vaccines. Effective protection can be achieved using egg-embryo propagated vaccine administered in drinking water to broilers.20 days. (Courtesy of the University of Georgia)
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. immature breeders and commercial pullets at 14 .neutralization. It is impossible to differentiate among the causes of respiratory diseases based on clinical observation only. LT may be transmitted to susceptible flocks or to unaffected areas following movement of vaccinates. The spray route is less effective especially with tissue-culture propagated vaccines. Commercial egg pullets and breeders are vaccinated at 6-10 weeks of age by administration of tissue-culture origin modified live virus which has a lower potential for reversion to virulence than chick-embryo origin vaccine virus.7 Prevention Strict biosecurity measures are justified in endemic areas. Detailed laboratory evaluation with identification of pathogens is required to confirm a diagnosis. 12.
67. Since flocks immunized with chick embryo origin virus serve as permanent carriers of the vaccine virus. ELISA serology may be used to confirm infection by demonstrating a significant rise in antibody in paired serum samples obtained during the acute and recovery phases of infection.
Broiler with swollen face and dyspnea due to laryngotracheitis.

Tracheitis which may be due to a range of viral agents including laryngotracheitis. D. Tripathy.
Caseous cast in the proximal trachea adjacent to the glottis is characteristic of laryngotracheitis but should be differentiated from diphtheritic pox infection and avian influenza.
Severe hemorrhagic tracheitis characteristic of infectious laryngotracheitis. N. avian influenza Newcastle disease or adenovirus. (Courtesy of Dr.
70. AAAP slide set)
69.68. infectious bronchitis. Specific laboratory procedures are required to establish a diagnosis.
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.

equipment and personnel and by wind dispersal of virus-laden dust and feathers.13. Flock morbidity is apparent following exposure to AI virus but mortality is variable depending on the pathogenicity of the strain of AIV and intercurrent climatic and environmental conditions. Sporadic outbreaks of HPAI result in severe losses in production. The virus is relatively resistant to environmental exposure and can infect birds placed in imperfectly decontaminated units housing a previously infected flock.
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.1 Etiology Diverse Type-A orthomyxoviruses characterized by hemagglutinating (HA) and neuraminidase (N) antigens occurring on the surface of the virus.0 AVIAN INFLUENZA 13.4 Clinical Signs Highly pathogenic avian influenza (HPAI) results in an acute and precipitous decline in egg production with rapidly ascending mortality characterized by both respiratory and nervous signs. 13. ultimately affecting all poultry operations in a region. Avian influenza viruses vary in their pathogenicity and their effects range from a mild respiratory disease (LPAI) to catastrophic losses associated with viscerotropic and pansystemic infection (HPAI or “fowl plague”). Rapid multiplication of HPAI virus occurs in susceptible subsistence and commercial flocks. This situation is common in countries with extensive distribution of live birds and where multi-age flocks are operated. 13. Avian influenza of low pathogenicity is an erosive disease reducing liveability and quality of either broilers or eggs and exacerbating secondary bacterial infection.3 Transmission Wild birds serve as reservoirs and transmit infection to subsistence flocks or commercial units which are operated with substandard biosecurity. Indirect infection can occur by moving flocks. Direct infection occurs following contact between infected carriers and susceptible flocks. Influenza adversely affects the financial return from flocks and a decline in quality of broiler carcasses or table-eggs following infection. disruption in operations and high costs for control and prevention.2 Occurrence and Economic Significance Avian influenza is world-wide in distribution. 13. unless appropriate controls are implemented.

7 Control in Areas Where Exotic HPAI is Diagnosed Exotic outbreaks of HPAI are eradicated by implementing an intensive program comprising rapid diagnosis. ND.5 Pathology Highly pathogenic avian influenza is characterized by subcutaneous hemorrhages and edema of the head.6 Diagnosis Rapid presumptive diagnosis is based on solid-state antigen capture assay (Directigen®) and confirmed by RT-PCR assay. flocks are immunized using autogenous inactivated vaccine or a recombinant vector product. pulmonary edema and if secondary bacterial infection occurs. Elevated mortality follows secondary E. denoting either exposure or vaccination. Studies in industrialized nations have shown that strict biosecurity can limit dissemination of avian influenza virus among commercial farms
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.Mild strains (LPAI) result in low morbidity and mortality. The agar-gel immuno-diffusion test and the ELISA procedure are used to demonstrate group specific AI antibody in serum. 13. AI viruses are then identified and serotyped using serumvirus neutralization followed by more advanced sero-immunologic procedures conducted in suitably equipped laboratories. An alternative but more time-consuming approach involves isolation of a hemagglutinating virus from tissues using specific pathogen free embryos or avian-cell tissue culture systems. Vaccination suppresses clinical occurrence of disease but the virus persists in the poultry population of the affected region. ILT. 13. quarantine and concurrent surveillance with subsequent disposal of flocks demonstrating antibodies to AI. slaughter and disposal of affected flocks. Vesicles may be present on the comb and wattles. In areas where inadequate resources or extensive dissemination of infection precludes absolute eradication. IB). Hemorrhages are observed in the serosa of all viscera and in the mucosa and lymphoid structures of the intestinal and respiratory tracts. airsacculitis is observed. 13. CA) and with concurrent respiratory pathogens (MG/ MS. Mild influenza results in tracheitis. and a decline in egg production. impeding exports. Restriction on movement of flocks and products from foci of infection should be imposed. coli infection superimposed on flocks with a history of exposure to immunosuppressive infections (IBD.

and within integrations. Preventing the spread of virus is extremely difficult in the context of industries in developing countries where feed is delivered in bags, and eggs, culled hens and live broilers produced by small-scale farmers are distributed through a network of dealers to regional markets. Since 1997, the zootiotic potential of AI has been recognized. Human fatalities associated with the 2004 outbreak of the H5N1 strain of AI in Southeast Asia has created international pressure for extensive vaccination to suppress infection in regions and nations where HPAI has resisted traditional eradication programs and has become endemic. 13.8 Recent Outbreaks of H5N1 Avian Influenza in Asia The 2003/2004 outbreak of H5N1 strain highly pathogenic avian influenza probably had its origins in China. Migratory waterfowl are considered to have introduced LPAI infection into free-living resident birds including sparrows and crows in the vicinity of feed mills and farms. These birds in turn transmitted virus to domestic subsistence chickens maintained under extensive management. Wild waterfowl may have also directly infected free-roaming domestic ducks and geese. Extensive movement of live domestic poultry to markets disseminated infection which eventually was introduced into large commercial operations. The H5N1 virus underwent mutation in large susceptible populations, resulting in a highly pathogenic agent. Spread of infection from China to Vietnam, Cambodia, Laos and Thailand was associated with unrestricted cross-border movement of live poultry including fighting cocks. Failure to recognize the infection and to implement appropriate control measures including quarantines, depletion of affected and contact flocks and vaccination has resulted in the development of endemic HPAI status in most countries in Asia where the disease has emerged. In Japan, Taiwan, Malaysia and Korea, limited outbreaks of H5N1 infection have been eradicated applying appropriate control measures for regions where the disease is exotic. China and Indonesia have adopted vaccination to suppress clinical outbreaks, recognizing this strategy to be the most cost-effective control measure. Asian outbreaks of H5N1 AI have been characterized by limited infection of humans following direct contact with diseased poultry. As of mid-2004 there have been no reports of direct human-to-human contact transmission. It is possible that a recombinant event between avian H5N1 and human influenza strains could occur in domestic swine or other animal species
89

yet to be identified in the chain of transmission. This could potentially result in a more pathogenic virus affecting humans, justifying vigorous suppression of infection in poultry populations and absolute separation of swine and poultry. Alternative strategies to control HPAI in countries with endemic infection should comprise detection and surveillance followed by depletion of infected flocks with fair compensation, quarantines and intensive vaccination appropriate to the circumstances. In the event of extensive spread of HPAI in a region, administration of a HA-homologous inactivated vaccine will reduce the proportion of susceptible birds in a population. This will inhibit the multiplication and dissemination of HPAI infection. The extent and severity of H5N1 infection in Asia presumes persistence of virus in reservoir populations, requiring a commitment to long-term vaccination and intensified biosecurity for commercial farms.

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71.

Subcutaneous hemorrhage characteristic of H5N2 strain of highly pathogenic avian influenza. (Courtesy of the University of Pennsylvania).

72.

Cyanosis of the head observed in cases of H5N2 strain highly pathogenic avian influenza. (Courtesy of the University of Pennsylvania).

73.

Severe hemorrhagic enteritis characteristic of highly pathogenic avian influenza or velogenic Newcastle disease. (Courtesy of the University of Pennsylvania).

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74.

Vesicle formation on the wattle of a bird infected with highly pathogenic influenza virus.

4 Clinical Signs Moderate morbidity and low flock mortality associated with respiratory rales (gurgling and snicking) and ocular discharge. Infection of immature chickens causes a mild respiratory disease which may affect liveability and growth if exacerbated by adverse managemental. The vaccination is repeated at 30-40 days.5 Pathology Hyperemia (red discoloration) of the trachea and accumulation of mucus in the nasal cavity.6 Diagnosis The diagnosis can be confirmed by immunofluorescence assay or isolation and identification of the causal virus using egg inoculation or tissue culture techniques.0 INFECTIOUS BRONCHITIS 14. RT-PCR is used to rapidly diagnose IB. 14. climatic stress or intercurrent mycoplasmosis. Retrospective diagnosis is possible by demonstrating a significant rise in circulating antibody in paired acute and recovery-phase sera applying ELISA or SN assay. 14. coli infection show airsacculitis. The initial live vaccine should always be administered to susceptible breeder and layer flocks before 12 weeks of age to avoid possible damage to the developing reproductive tract of
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.2 Occurrence and Economic Significance Infectious bronchitis (IB) occurs world wide and is responsible for depressed egg production and shell quality in susceptible commercial and breeder flocks. Massachusetts.7 Prevention Immature breeders and commercial layer flocks are routinely vaccinated with a mild attenuated product (H-120. Mature flocks show reduced egg production with malformed shells. 14.1 Etiology Specific strains of an avian coronavirus. Where suitably equipped laboratory resources are available. 14. complicated by secondary E.3 Transmission The virus can be transmitted from clinically affected birds to susceptible flocks either by direct contact or indirectly by fomites. 14. 14.14. Chronic cases. Connecticut strains or their combination) at 7 days in drinking water or by aerosol.

Potential breeder flocks receive inactivated IB vaccine as a booster. to maintain adequate maternal antibody transfer to progeny.
94
.the pullet. Broilers in endemic areas are vaccinated by aerosol at day-old or subsequently by coarse spray or in drinking water at a suitable time (1020 days) depending on maternal antibody transfer or pattern of field challenge. usually in the form of an injectable multivalent emulsion at the end of the rearing period and then at mid-cycle. Immunity in commercial layers can be boosted by administration of live attenuated vaccine either in drinking water or as a coarse spray during the production period. as considered necessary. In many areas specific IB vaccines are required to prevent clinical problems attributed to variant strains.

3 Transmission Mycoplasmosis is transmitted by the vertical route from infected parent flocks to progeny. synoviae are the two significant species affecting commercial chickens. 15. and personnel.15. Wild birds and rodents may transmit the disease to susceptible flocks. These conditions are responsible for extensive losses in broiler operations especially where flocks are exposed to concurrent viral respiratory diseases and environmental stress. 15. Chronic cases are emaciated and show purulent nasal discharge. and condemnation at processing.4 Clinical Signs Mycoplasmosis is characterized by chronic respiratory signs including ocular discharge. synoviae infection results in acute arthritis especially of the hock and stifle joints. The economic impact of mycoplasmosis in broilers includes severely depressed growth rate and feed conversion efficiency. Indirect infection occurs through contact with contaminated equipment.
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. 1 Etiology Mycoplasma gallisepticum and M. Mycoplasmas do not survive outside the host for longer than 24 hours. feed bags. synoviae infection. markedly reduced growth rate and an increased susceptibility to intercurrent respiratory diseases.0 MYCOPLASMOSIS 15. M. 15. gallisepticum and synovitis and airsacculitis due to M. elevated mortality. tracheal rales (“gurgling and snicking”). In commercial layers and breeders. occur world-wide. Lateral transmission occurs by direct contact between clinically affected or recovered carriers and susceptible flocks. liveability and egg production are depressed.2 Occurrence and Economic Significance Chronic respiratory disease caused by M.

Strict biosecurity will prevent lateral introduction of infection. Kits are available for M. Chicks derived from known infected parent flocks can be treated with a suitable antibiotic during the first 48 hours after placement and re-treated subsequently at 20 to 24 days of age for a 24 to 48 hour period. infected layer farms. Mycoplasma spp can be isolated and identified by inoculating tracheal swabs or serous joint exudate from acute cases onto special selective media. It is emphasized that treatment does not eliminate the carrier state in infected flocks but will suppress excretion of the organism in respiratory exudate and vertical transmission through eggs. The polymerase chain reaction assay can be applied as a commercially available. In advanced cases. 15.15. The hemagglutination inhibition test is applied to confirm the provisional serologic diagnosis. Live M. synoviae respectively. sensitive and specific test procedure. gallisepticum and/or M. Inactivated vaccines administered as oil emulsions are available commercially but
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. 15. Acute cases of M. synoviae infection show serous arthritis. These highly sensitive tests are used to screen flocks. gallisepticum vaccines are available for immature egg-production flocks which will be transferred to multi-age. The liveattenuated F-strain vaccine administered in drinking water has been largely replaced in the USA by the milder TS-11 and 6/84 products. Infection of grandparent and parent level breeders occurs in developing industries due to deficiencies in biosecurity on farms operated by multipliers.5 Pathology Affected birds show congestion of the upper respiratory tract. This procedure may require up to 30 days and may be inconclusive due to technical problems including contamination.6 Diagnosis Two to three weeks following infection. mild tracheitis. and in chronic cases airsacculitis and colibacillosis.7 Treatment Clinical signs can be suppressed by administering tylosin or a fluoroquinolone compound in drinking water.8 Prevention The world’s primary breeders of broilers and commercial layers have eliminated mycoplasmosis. seropurulent exudate may be present in affected joints. It is essential to purchase parent and commercial stock from known mycoplasma-free breeder flocks. chickens demonstrate antibodies which can be detected using the serum plate agglutination test or the automated ELISA technique. 15.

It is noted that vaccination will suppress clinical signs of infection but will not eliminate the carrier state.are of limited value. A pox-vectored recombinant Mg vaccine (“Vectormune”) has recently been licenced for administration to immature egg-production pullets in the USA.
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.

Mortality is negligible in uncomplicated cases of coryza. 16.0 CORYZA 16. 16.1 Etiology Three Haemophilus paragallinarum serotypes designated A. 16.16. The pathogen does not remain viable outside the host for periods exceeding 24 hours.7 Treatment Immature birds can be treated with water-soluble sulfonamides. 16.4 Clinical Signs Flock morbidity varies from 1 to 20%. B and C are recognized. Egg production in young commercial or breeder flocks is reduced following infection. These
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. incubated in a candle jar.2 Occurrence The disease is potentially encountered in any poultry-raising area but frequently occurs in specific regions or countries as a chronic or seasonal problem. The condition should be differentiated from pasteurellosis and viral infections including LPAI. Alternatively. Isolation involves semiaerobic culture on a blood agar medium streaked with Staphylococcus sp. 16. Chronic cases show serous to caseous sinusitis. and other respiratory agents. severed heads packed on ice can be forwarded to a laboratory.5 Pathology Acute cases show severe conjunctivitis and inflammation of the periorbital fascia.3 Transmission Infection follows direct contact with clinically affected or asymptomatic carriers or indirect contact with contaminated equipment or personnel. Coryza results in decreased egg production in commercial multiage laying and breeder operations.6 Diagnosis Haemophilus paragallinarum can be isolated from sinus swabs in acutely affected birds. 16. Clinically affected birds show unilateral or bilateral ocular discharge progressing to facial cellulitis and chronic sinusitis. Since the organism is susceptible to desiccation it is recommended that acutely infected live birds should be submitted to a diagnostic laboratory whenever possible.

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. 16. Ocular discharge and swelling of the nasal sinus associated with Coryza.
80.
Accumulation of purulent material in the infraorbital sinus is characteristic of coryza. Differential diagnosis includes mycoplasmosis or laryngotracheitis. Two doses of inactivated vaccine should be administered by the subcutaneous or intramuscular route at four week intervals during the rearing period. Immature flocks can be partly protected by administration of inactivated multivalent or homologous bacterins in aqueous suspension or oil emulsion.
79. as recommended by the manufacturer.8 Prevention Appropriate biosecurity measures will limit the possibility of introducing infection on to breeding and commercial egg production farms. Combinations of tetracyclines are frequently used to treat coryza by administration in water or injected directly by the intramuscular route.drugs should not be administered to mature flocks due to residues in eggs and the deleterious effect of sulfonamides on production and shell quality. Compulsory or recommended withdrawal periods before marketing eggs should be followed after treatment of commercial flocks.

1 Etiology Various fungi including Aspergillus fumigatus. Horizontal transmission can occur in the hatchery or during handling and delivery. Mycotic encephalitis (infection of the brain) results in lateral recumbency. 17. Confirmation of the diagnosis requires culture using an appropriate fungal medium (Sabouraud’s dextrose agar).0 ASPERGILLOSIS synonym Mycotic Pneumonia 17.7 Prevention Improving nest-box hygiene. This is followed by subsequent infection of the respiratory tract of pipping embryos and hatching chicks. incoordination and coarse muscle tremors. Histological examination of lungs will reveal characteristic hyphae.5 Pathology Numerous 1mm diameter yellow to green nodules are observed in the lungs and air sacs and occasionally in other organs including the brain and eye.4 Clinical Signs Morbidity may attain 10% of the flock with corresponding mortality during the first 3–12 days. frequently accompanied by a whistling rale. 17. Chicks older than 48 hours are usually refractory to infection by inhalation of spores.2 Occurrence and Economic Significance The disease is world-wide in distribution but cases are more frequently diagnosed in tropical countries especially during warm and humid weather. Decreased growth rate and ascites complex are noted in affected survivors. 17. 17. 17.6 Diagnosis Characteristic lesions are highly suggestive of aspergillosis.17. increasing the frequency of collection of
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. Severe outbreaks associated with hatchery contamination may result in up to 15% chick mortality during the first two weeks. Affected chicks are disinclined to move and show labored breathing with extension of the head. 17.3 Transmission Contamination of egg shells with Aspergillus spores results in colonization of the air cell.

substituting plastic nest pads for litter will reduce the prevalence of aspergillosis. Decontamination of setters.eggs to four times daily and where possible.
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. but eggs should not be washed by immersion. Decontamination of eggs by formalin fumigation or application of a QAT or phenolic disinfectants is advised. using an appropriate microbiological detection procedure such as an air sampler or exposed petri-plates. and air ducts is recommended including the use of aerosol generators and medicated “candles.” The efficacy of cleaning procedures can be monitored. hatchers.

82.81.
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.
Severe pulmonary aspergillosis showing numerous nodular foci and confluent lesions.
Multiple fungal granulomata typical of aspergillosis.
Diffuse airsacculitis of the thoracic air sacs and focal airsacculitis and peritonitis due to aspergillosis in a young chick.
83.

and Latin America. ND) and terminating in E. 18. Regionally. Asia. coli cellulitis of the subcutaneous tissues surrounding the eyes and of the head. eyes are closed and enlargement of the head is a prominent sign in severely depressed or recumbent broilers. 18. Environmental stress (low temperature and humidity. coli or other opportunistic pathogens including Ornithobacterium rhinotracheale (ORT) can be introduced through contaminated water and litter. 18. or high dust and ammonia levels) due to inadequate ventilation or climatic extremes exacerbate the prevalence and severity of SHS. Subsequent bacterial septicemia and airsacculitis which occur approximately 10 .0 SWOLLEN HEAD SYNDROME 18. the Middle East. Related metapneumoviruses including turkey rhinotracheitis virus (TRT) causing tracheitis and sinusitis in turkeys and a swollen head condition in broiler breeders are accepted as a precipitating agent of SHS in broilers. coli strains. SHS often shows a seasonal (winter) occurrence. TRT.14 days after the onset of acute facial cellulitis may result in additional flock mortality of up to 20% of survivors of an acute outbreak.3 Transmission The immune suppressive and respiratory agents are transmitted by direct and indirect contact and usually are associated with defects in biosecurity. Pathogenic E. especially on multiple-age farms. Terminally. Affected birds show ocular discharge and conjunctivitis progressing to periorbital swelling.4 Clinical Signs Under commercial conditions SHS is characterized by acute onset of morbidity involving up to 10% of the flock in broilers aged 14 . MD.2 Occurrence and Economic Significance The condition occurs in southern Africa. Pathogenic E. usually introduced through contaminated drinking water are responsible for the subcutaneous facial and occipital cellulitis which is characteristic of SHS. Outbreaks of facial cellulitis in chickens have been diagnosed in California without evidence of metapneumovirus infection. Losses due to primary mortality may attain 10% to 20% of the flock. especially in high-density broiler growing areas. CA) followed by exposure to a respiratory virus (IB.
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.18.1 Etiology Swollen Head Syndrome (SAS) is a multifactorial condition involving the sequence of immune suppression (IBD.30 days.

Chronic cases show caseous airsacculitis. In small-scale operations acute cases can be salvaged by transfer to small pens where food and water are available and birds can be treated with parenteral antibiotic and protected from persecution by the remainder of the flock. coryza.5 Pathology Subcutaneous accumulation of viscous sero-purulent exudate. Improper or prolonged use of antibiotics will result in emergence of drug-resistant E.18.6 Diagnosis The obvious gross lesion comprising subcutaneous cellulitis of the head is highly suggestive of SHS. Acutely affected birds may show tracheal hyperaemia and pulmonary congestion. pasteurellosis. Bursal and thymic atrophy consistent with previous IBD or CAV infection.8 Prevention Chlorination of drinking water to 2 ppm and installation of closed (nipple) drinking systems are recommended. coli. Attempts to isolate and identify primary viral pathogens and secondary bacterial pathogens should be carried out. respectively. 18. Differential diagnoses include LPAI. Alleviation of obvious managemental deficiencies and environmental stress factors will reduce the intensity of respiratory stress. Antibiotics should be used in accordance with the manufacturer’s instructions and statutory restrictions relating to the withholding period before slaughter should be observed. Losses frequently resume after withdrawal of medication. Appropriate vaccination programs are required to prevent immunosuppressive and respiratory viral diseases.
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. ND. Serologic profiling of flocks is necessary to determine the pattern of maternal IBD antibody decay and the response to either vaccination or field challenge with a range of respiratory and immunosuppressive agents. which becomes caseous in chronic cases. 18. may be apparent. perihepatitis and peritonitis. IB.7 Treatment Administration of water soluble antibiotics including fluoroquinolones will produce a transitory decline in flock mortality. 18. Medication should be guided by anticipation of a positive benefit:cost ratio.

IB by vaccination and improved flock management and provision of chlorinated drinking water will reduce losses.
84.Breeders can be vaccinated with commercial metapneumovirus vaccines. S. Buys)
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. Attempts at immunization of broilers have not been successful. Control of IBD. (Courtesy of Dr. ND.
Swollen Head Syndrome in broiler showing cellulitis of the face and head with symblepharon (closed eyes).

2 Occurrence and Economic Significance Septicemia and airsacculitis resulting from E. resulting in downgrading or condemnation at processing. superimposed on primary immunosuppressive and respiratory viral infections.0 SEPTICEMIA AND AIRSACCULITIS 19. coli. enlargement of the spleen and liver. pericarditis and peritonitis. Flocks infected with vertically transmitted or acquired mycoplasmosis are extremely susceptible to E. Infection of commercial laying and breeding stock during the rearing period may adversely affect subsequent performance. coli is introduced onto poultry farms through contaminated drinking water. Total losses may attain 50% in immunosuppressed broiler flocks subjected to environmental stress and previous exposure to viral respiratory pathogens and mycoplasmosis. High levels of infection occur following deficiencies in routine decontamination of housing. and generalized venous congestion. Diets containing aflatoxins or free radicals evolved from peroxidation of lipids will lead to immunosuppression with increased susceptibility to E.4 Clinical Signs Flock morbidity of up to 10% occurs during the 10 – 40 day period accompanied by ascending mortality which may either plateau or decline but usually persists until depletion of the flock.1 Etiology Pathogenic strains of E. Most birds which die of septicemia show perihepatitis. coli airsacculitis.5 Pathology Acute septicemia is characterized by pulmonary congestion.
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. Immunosuppressive and respiratory viruses which precipitate infection are transmitted by direct and indirect contact especially on multi-age farms or where biosecurity is defective.19. 19. 19. equipment and drinking systems. elevated flock mortality. 19. coli infection are responsible for decreased growth rate and feed conversion efficiency. coli infection.3 Transmission E. Bursal atrophy indicating previous exposure to IBDV is often observed. downgrading and condemnation of carcasses in processing plants. Birds surviving acute airsacculitis show stunted growth and develop a caseous exudate in the air sacs often accompanied by peritonitis. 19.

Evaluation of the epidemiology of immunosuppressive and respiratory infections by serology and isolation is recommended.
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. 19.
Grossly enlarged yolk-sac of a chick showing redtinged contents associated with omphalitis. and liver tissue. identification and serotyping of E. Swollen Head Syndrome. coli from heart blood. 19. Medication should be administered in accordance with statutory restrictions concerning withdrawal and must comply with the manufacturer’s recommendations.6 Diagnosis Isolation.7 Treatment Mortality can be suppressed by administration of water soluble furazolidone. Hand cleaning of hatching eggs is an undesirable practice and leads to “exploders” in setters and hatchers and omphalitis in chicks due to bacterial contamination. sulfonamides.
85. perivisceral exudate. It is necessary to perform antibiograms to ensure that selected drugs are effective.8 Prevention Refer to 18.19.8. and fluoroquinolones where these drugs are permitted.
86.

88.
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.
Chronic salpingitis occurs frequently in old breeder hens and is probably due to an ascending E.
Pericarditis which is usually associated with E.
Enlarged yellow yolk-sac. coli infection of the oviduct. coli infection.
89. typical of omphalitis in a 3 day old chick.87.

litter. housing. Omphalitis is often present. The pathogen can remain viable in soil for up to a year. 20. Affected chicks are depressed and anorexic and tend to huddle under brooders. liver) and chronic caseous typhlitis characterized by grey casts in the ceca. and clothing of personnel. BWD) is potentially world-wide in distribution but in practice is confined to non-commercial flocks in many countries. Infection results in high mortality in young chicks. Chronic cases show abscessation of the viscera (heart. pullorum from liver. 20.3 Transmission Vertical transmission occurs by the transovarial route. poor feathering and frequently lameness due to arthritis.1 Etiology: Salmonella pullorum 20.20. 20. intestine or yolk sac using appropriate enrichment culture and standard microbiological techniques. lungs. Birds may show copious white diarrhea and accumulation of fecal material adherent to the plumage surrounding the vent. Recovered carriers can be identified using the rapid whole blood plate agglutination test.5 Pathology Chicks show enlargement of the spleen and liver. internal serosa.4 Clinical Appearance Morbidity in affected batches of chicks often exceeds 40% with corresponding mortality commencing at hatch and extending through 21 days.
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. From 14 days of age onwards affected birds show stunting. 20.2 Occurrence and Economic Significance Pullorum disease (or “bacillary white diarrhea”.0 SALMONELLOSIS-PULLORUM DISEASE 20.6 Diagnosis Isolation and identification of S. Horizontal transmission takes place by direct contact between clinically affected and recovered carriers and by indirect contact with contaminated equipment.

8 Prevention Breeding stock and chicks should be purchased from suppliers and hatcheries certified free of S. pullorum by a responsible government agency. Breeder flocks can be monitored using the rapid whole-blood plate agglutination test.
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.7 Treatment None is recommended. 20. Affected flocks should be depleted to eliminate chronic carriers.20. Strict biosecurity should be enforced to prevent introduction of the pathogen from backyard flocks which serve as reservoirs. Rodent eradication is an important component of control.

3 Transmission Vertical and lateral transmission occurs as for S.10% within a week. Commercial laying flocks may be salvaged under specific conditions by administering furazolidone or tetracycline in feed at 400 g/ton. 21. Eggs should not be marketed during medication or the subsequent withdrawal period. Diarrhea.7 Treatment Treatment is inappropriate for breeding flocks.6 Diagnosis Isolation and identification of S.21. 21. No characteristic prodromal signs are noted.
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. gallinarium is required to confirm the diagnosis. for two weeks. Producers in Latin America and Asia experience mortality in both mature and immature flocks.2 Occurrence and Economic Significance Potentially world-wide in distribution and frequently encountered in subsistence or semi-commercial flocks. 21.0 SALMONELLOSIS-FOWL TYPHOID 21. The disease is responsible for serious economic losses in commercial units in organized poultry industries in endemic areas. depression and a decline in egg production are observed in mature flocks but these signs are not diagnostic. Oophoritis (inflammation of the ovary) followed by ovarian regression is noted in mature stock.5 Pathology Gross enlargement of the spleen and liver are observed in affected cases. 21. The rapid whole blood plate agglutination test will demonstrate antibodies approximately 2 weeks after infection and can be used to screen flocks for reactors. which should be depleted. where permitted. pullorum. Ascending morbidity and corresponding mortality may attain 5 .1 Etiology: Salmonella gallinarum 21. Peritonitis may be present in chronic cases. 21.4 Clinical Signs Acute onset of fowl typhoid occurs in susceptible flocks which are exposed to infection. loss of egg production and increased costs incurred by prevention and treatment.

21.
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. pullorum infection. Bacterins are generally ineffective in preventing fowl typhoid. to prevent introduction of infection. gallinarum vaccine during the rearing period will eliminate outbreaks of clinical disease. Administration of live 9R strain S.8 Prevention Appropriate biosecurity measures should be implemented as for S.

5 Clinical Signs Elevated chick mortality and unevenness in brooding flocks are observed. Paratyphoid Salmonella spp are responsible for food-borne infection in consumers of eggs (S. agona.22.
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.1 Etiology Salmonella spp other than S. infrequently by the transovarial route. S. Paratyphoid salmonellosis can be introduced by contaminated equipment. gallinarum.6 Pathology Acute cases show enlargement of the spleen and liver and occasionally enteritis and peritonitis. Vertically transmitted S.3 Economic Significance Some Salmonella spp including S. Enteritidis) and poultry meat (S.4 Transmission S. heidelberg and possibly up to 50 other frequently encountered serotypes). may result in high chick mortality consistent with S. 22. Generally paratyphoid Salmonella spp will result in up to 3% losses during the first 14 days. enteritidis is transmitted vertically by the trans-ovarial and transoviductal routes. The condition can be perpetuated by recycling contaminated by-product meal from infected broilers and commercial laying flocks. phage type 4. S. enteritidis. Feed containing contaminated ingredients of animal-origin is often responsible for introduction of paratyphoid salmonellosis into integrations or entire countries. Other Salmonella spp may be transmitted mechanically by fecal contamination of egg shells. 22. enteritidis pt 4 infection resembles pullorum disease in chicks. pullorum and S. or in cases of immunosuppressed flocks. Chicks may show omphalitis.2 Occurrence A world-wide problem in integrated commercial-egg and broiler operations and also on small-scale farms.0 SALMONELLOSIS-PARATYPHOID 22. Rodents and litter beetles serve as reservoirs of infection. 22. typhimurium. 22. personnel and wild birds. Pullorum infection. 22. No specific signs are associated with paratyphoid infection in mature flocks.

enteritidis emulsion boosters at point of lay. intestine. typhimurium vaccines alone or in combination with inactivated S. enteritidis antibody. spleen.9 Prevention Reduction in prevalence in breeding flocks is possible (absolute elimination of S. modified S. 22. Specific ELISA-based test kits are available for assaying for S. Routine microbiological screening of liver/spleen/intestinal pools from post mortem submissions to laboratories is strongly recommended. Enteritidis and progressively S.8 Treatment Furazolidone if allowed will suppress mortality but will not eliminate infection.22.7 Diagnosis Confirmation is based on isolation and identification of Salmonella spp from liver. typhimurium carriers) by implementing intensive programs of microbiological screening together with appropriate biosecurity procedures. 22.
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. or heart blood. Salmonella enteritidis is controlled in commercial level stock using live.

90.
91.
Accumulation of urate and excreta in the vicinity of the vent in chick with Salmonella pullorum infection. hence the designation “Bacillary White Diarrhea” (BWD) in the British commonwealth.
Regression of the ovary in a mature hen due to Salmonella pullorum infection. This change is not characteristic of salmonellosis but may be observed with a number of bacterial infections including E. coli and Pasteurella spp. (Courtesy of the University of Georgia)
92.
Enlargement of the liver with Salmonella gallinarum (Fowl Typhoid).
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.

93.

Panophthalmitis in a turkey poult is characteristic of Salmonella arizona infection, but may occur with S. pullorum in chicks.

94.

Multiple focal abcessation of the liver and heart following Salmonella gallinarum infection. These changes may also be seen with S. pullorum.

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23.0 PASTEURELLOSIS synonym Fowl Cholera 23.1 Etiology Pasteurella multocida serotypes (including 1, 3, & 4) which vary in pathogenicity. 23.2 Occurrence and Economic Significance World-wide in distribution, pasteurellosis is encountered as an endemic infection in many intensive poultry producing areas and frequently persists as an infection in specific integrations or farms. Mortality occurs in floorhoused replacement commercial laying and breeding stock and extends into mature flocks. Acute outbreaks associated with environmental or managemental stress, may result in depression in egg production. In breeders, reduced mating activity lowers fertility and depresses productivity of flocks as measured by the number of chicks produced by each hen placed. 23.3 Transmission Infection occurs following direct contact between susceptible birds and clinically affected or recovered carriers. Environmental contamination, rodents, and wild birds are sources of indirect infection. Contaminated feed bags, equipment, and the clothing of personnel may introduce infection onto farms or into integrations. Intraflock transmission is enhanced by handling birds for vaccination and weighing and by open watering systems such as troughs and bell drinkers. 23.4 Clinical Signs Morbidity and mortality rates depend on the pathogenicity of the strain and the susceptibility of the flock. Newly introduced infections may result in up to 10% mortality. Prodromal signs are not observed in peracute cases. Chronic infection may be recognized by enlargement of the wattles, lameness caused by arthritis and torticollis (twisted necks) due to otitis interna (infection of the inner ear). 23.5 Pathology Acute cases show enlargement of the spleen and liver with punctate hemorrhages of the viscera including the heart. Subacute cases may show gray granulomatous foci in the liver. Caseous cellulitis of the wattles and seropurulent arthritis may be present in chronic cases.

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23.6 Diagnosis Laboratory examination is required to isolate and identify P. multocida from specimens of heart blood, liver, and spleen. In acute cases, characteristic bipolar organisms may be observed in Giemsa-stained smears of heart blood. 23.7 Treatment Tetracycline incorporated into feed at a level of 200 - 400 g/ton or in water at 250 - 500 mg/l will suppress clinical signs and reduce mortality. 23.8 Prevention Stringent biosecurity procedures are necessary to prevent introduction of infection. Eradication of rodents is critical to reducing the exposure of flocks to P. multocida. Immunization of flocks in endemic areas is recommended. Routine vaccination is essential on farms where previous cases have occurred. Live-attenuated P. multocida vaccines (CU; PM-1; PM-9 strains) are administered by wing-web stab twice during the rearing period, at approximately 10 and 14 weeks of age. Breeder males or flocks subjected to environmental stress may be vaccinated with the relatively milder PM1 and PM-9 strains in place of the CU strain to avoid adverse vaccine reaction. Antibiotics should not be administered one week before and one week after administration of a live attenuated vaccine. Inactivated vaccines can be used to protect flocks if an undesirable reaction to a live vaccine occurs. It is emphasized that for effective control of pasteurellosis inactivated bacterins must be homologous with the endemic strains of P. multocida. In some areas or integrations, autogenous, inactivated vaccines are required.

Torticollis in a hen which might be due to infection of the inner ear by E. coli or Pasteurella multocida. This change is also observed in flocks exposed to velogenic Newcastle disease.

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24.0 SPIROCHETOSIS 24.1 Etiology A spirochete, Borrelia anserina. 24.2 Occurrence and Economic Significance Spirochetosis is widespread in tropical countries due to the prevalence of the soft-shell tick vector Argas spp. The condition is responsible for sporadic losses in subsistence flocks and small scale commercial units. 24.3 Transmission Ticks of the genus Argus are most frequently implicated in transmission of spirochetosis. Studies have confirmed that mites including Dermanyssus spp and Culex spp mosquitoes may also be involved in transmission. 24.4 Clinical Signs Young birds are apparently more susceptible than older stock. Acutely affected birds show depression with cyanosis (blue discoloration) of the head. Mortality may attain 30% of the flock. In sub-acute and chronic cases, birds show paresis (weakness) terminating in paralysis and death. 24.5 Pathology A grossly enlarged spleen with mottling due to subcapsular hemorrhage is the predominant lesion. Focal necrotic hepatitis may also be present. 24.6 Diagnosis Demonstration of the organisms in Giemsa-stained blood smears. The pathogen can be propagated from a spleen homogenate injected into the yolk sac of embryonated eggs at the 6th day of incubation. 24.7 Treatment Oxytetracycline by injection (1-2 mg/kg body weight) or chlortetracycline in drinking water are effective. 24.8 Prevention Eradication of vectors and dusting birds at frequent intervals with 5% carbamate (Sevin®) powder. In some countries, locally prepared vaccines are available but vary in efficacy.

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Lymphoid aggregations are observed in the proventriculus. Affected chicks show depression progressing to prostration in lateral recumbency. and feet.7 Prevention A live-attenuated vaccine can be administered to replacement commercial laying and breeding stock during the 10 . AE 25.3 Transmission Vertical transmission occurs by transviral passage of virus from viremic hens to their progeny. 25. 25.4 Clinical Signs Mortality occurs in chicks aged 3 .2 Occurrence and Economic Significance Avian encephalomyelitis (AE) occurs world-wide.5 Pathology No gross lesions are observed. pancreas and other organs. Commercial ELISA test kits are available to monitor the antibody titer of flocks to determine susceptibility or following vaccination or challenge. Recovered birds may show lenticular opacity (cataracts). 25.20 days. resulting in an asymptomatic egg production decline in commercial layers and breeders and elevated mortality in vertically infected batches of chicks. Terminally.14 week period. chicks demonstrate fine muscular tremors of the head.0 AVIAN ENCEPHALOMYELITIS synonyms Epidemic tremor. Lateral spread from birds which shed AE virus in feces results in direct and indirect infection of susceptible flocks. 25. neck.25. Morbidity varies according to transmission rate but seldom exceeds 5% under commercial conditions.
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. Infection of susceptible breeder or commercial egg flocks results in an asymptomatic decline in egg production.6 Diagnosis Histological examination of brain and spinal cord tissue reveals perivascular cuffing and degeneration of neurons.1 Etiology: A picornavirus 25. 25. especially in areas where AE vaccination is an accepted practice. Epidemic tremor virus can be isolated from brain tissue by inoculation of embryonated SPF eggs. This is important in differentiating AE from encephalomalacia.

Vaccines are available for administration in drinking water or as a combination product with avian pox using the intradermal. Lateral spread of vaccine virus will result in a drop in egg production in susceptible hens and mild outbreaks of epidemic tremor in progeny. (Courtesy AAAP)
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. Care should be taken to avoid introducing AE vaccine onto multi-age breeder farms. wing-web stab route.
98. Detailed laboratory examination including histopathology is required to obtain an accurate diagnosis. nutritional encephalomalacia or arenavirus infection (Spiking Mortality Syndrome). avitaminosis A. For the same reason. pullets should not be vaccinated after 12 weeks of age since intestinal shedding of vaccine virus can occur for at least 4 weeks following vaccination.
Incoordination and lateral recumbency in a chick which may be due to avian encephalomyelitis.

4.4.4 Adenoviral Respiratory Infection 26.1 Clinical Signs Mild respiratory signs (moist rales) occur in a few birds in a flock following infection.0 ADENOVIRAL INFECTIONS 26. Vaccines produced using infected. This infection has not been diagnosed in the USA and Canada. Inclusion body hepatitis and mild adenoviral respiratory infection may occur in all areas where commercial chickens are reared. Pakistan (Angara disease). 26. Asia. Indirect infection is possible on contaminated personnel. and Latin America and is emerging as a significant restraint to production in areas where intercurrent problems of immunosuppression due to vvIBD and vvMD occur.
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. inclusion body hepatitis and hydropericardium-hepatitis syndrome (HHS) in chickens. 26. The condition is characterized by slow onset and spread within and among flocks.2 Pathology Mild inflammation of the tracheal mucosa is observed following primary infection. Egg-drop syndrome in chickens. non-SPF embryos have been implicated in outbreaks of EDS and HHS in Asia. Hydropericardium-Hepatitis syndrome is responsible for severe losses in India (Lychee disease).
26.26. Africa. and Latin America. 26. equipment and housing. Under commercial conditions.2 Occurrence and Economic Significance Egg drop syndrome in mature flocks occurs in Europe. direct transmission occurs from fecal shedders to susceptible flocks.1 Etiology Type 1 adenovirus:
Type 2 adenovirus: Type 3 adenovirus:
Different strains produce specific conditions including mild respiratory infections. Hemorrhagic enteritis of turkeys.3 Transmission All adenoviruses are potentially transmitted by the vertical route.

no specific clinical abnormalities can be detected following direct or indirect exposure to EDS virus.5.3 Diagnosis Isolation and identification of the causal agent using SPF eggs. with ruffled plumage and are disinclined to move.20%) morbidity and slightly elevated mortality occur in broilers and replacement rearing and breeding flocks aged 2 . 26. No specific vaccine is available. 26.3 Diagnosis Histological examination of affected livers often shows intranuclear inclusions. with mottling due to petechial hemorrhages under the capsule interspersed with areas of necrosis.1 Clinical Signs Moderate (5 . Effective control of Marek’s disease and IBD together with early exposure of breeders to mild prevalent adenoviral strains have contributed to a decline in the severity of adenoviral inclusion body hepatitis in broiler flocks in the USA.6 weeks.4 Prevention No specific vaccine is available. 26.1 Clinical Signs Other than acute drop in egg production in mature flocks. Specific inactivated oil-emulsion HHS vaccines are available for administration in endemic areas. Adenovirus can be isolated from the respiratory and digestive tracts by inoculating embryonated SPF eggs. morbidity and mortality may exceed 10%. 26. characterized by enlargement of the kidneys and urate retention may be observed in chronic cases. Eggs produced by brown and tinted-shelled strains show
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.26.5. Nephrosis. No specific clinical signs are demonstrated.5 Inclusion Body Hepatitis 26. The more severe HHS infection is characterized by hydropericardium and focal hepatic necrosis.6.5.4. 26.2 Lesions Enlargement of the liver. In the presence of intercurrent immunosuppressive viruses. Affected birds are depressed. 26.4 Prevention All-in-all-out placement programs and appropriate biosecurity procedures are recommended.4.6 Egg Drop Syndrome 26.5.

6.4 Prevention Vaccination of immature breeding and laying flocks with an inactivated oil-emulsion vaccine is recommended before onset of production.lack of pigment and shells have a “chalky” appearance. Histological changes in the oviduct occur following infection. Confirmation of a diagnosis is based on demonstrating a rise in antibody titer in paired sera applying VN or ELISA procedures. Failure to attain peak production may be associated with activation of latent infection or lateral introduction of infection at onset of sexual maturity. 26.6. 26.2 Lesions Examination of sacrificed. clinically unaffected birds will show regression of the ovary. 26.
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.6.3 Diagnosis Isolation of the causal virus in duck eggs or on liver cell tissue culture.

Infectious Stunting Syndrome 27. 27.0 RUNTING SYNDROME synonyms Malabsorption. It is noted that the condition can be reproduced by infecting specific-pathogen free chicks with intestinal homogenates from affected birds. It is known that reovirus infection can remain latent in replacement pullets during the rearing stage with viremia appearing at the onset of production and persisting for approximately 4 to 6 weeks thereafter. through 30 days of age. It is not possible to reproduce the typical stunting syndrome by administering reovirus isolates from field cases. loose droppings from infected birds shows the presence of undigested grain particles. The severity and prevalence of the condition generally abates within 1 to 2 years after initial appearance in an area. affected chicks which may comprise up to 25% of the flock may weigh only 250 g and are less than half the size of normal pen mates.3 Transmission The reovirus presumed to be responsible for the condition is transmitted by the vertical route from infected hens to progeny in addition to lateral infection among broiler chicks.27. suggesting a multifactorial etiology. possibly in association with as yet unidentified viruses or anaerobic bacteria in the intestinal tract. 27.1 Etiology: The specific causal agents responsible for Stunting Syndrome have not been identified. 27. By 4 weeks of age. In extreme cases fracture of the proximal epiphysis of the
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.4 Clinical Signs Affected chicks show decreased growth rate which is evident by the 5th to 7th day of brooding. Feather abnormalities are obvious in affected chicks and include breakage of the shafts of the primary feathers of the wings and persistence of yellow down on the head.2 Occurrence and Economic Significance The condition has been diagnosed in most broiler-raising areas and is responsible for decreased growth rate and elevated mortality in broiler chicks usually derived from young parent flocks. although most poultry health professionals accept that specific reovirus strains (including 1733) are responsible for the condition. Abnormal wing feathering gives rise to the term “helicopter disease” since the abnormal feathers resemble rotor blades. A high proportion of affected birds show a disinclination to walk due to a rickets-like syndrome characterized by osteopenia. Examination of the orange-colored.

osteopenia resulting in fracture of the proximal epiphysis of the femur (incorrectly termed “femoral head necrosis”). Evaluation of dietary formulations is advised to ensure nutritional adequacy. 27. enteritis is not a primary lesion although affected birds may be concurrently infected with coccidiosis or may undergo secondary bacterial infection. 27. Isolation of affected chicks may reduce the probability of lateral transmission of virus. These changes which are observed clinically are confirmed on post-mortem examination. Despite obvious malabsorption. The following components should be considered: • levels of methionine and lysine should attain or exceed breed specifications
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. and can be salvaged for live-bird sale or processing as lowweight birds.femur occurs. beading of the ribs. There are no characteristic gross or histological lesions associated with the stunting syndrome. Since the range of etiologic agents have not been identified. 27.6 Diagnosis A diagnosis of stunting syndrome is based on the history of young parent flocks producing affected chicks and the appearance of up to 20% stunting in a flock with typical clinical presentation in affected birds ranging in age from 7 to 35 days.7 Treatment There is no specific treatment for stunting syndrome.5 Pathology Stunting syndrome attributed to malabsorption is characterized by a wide range abnormalities including: • A rickets-like syndrome involving decreased skeletal density. Affected chicks can be gathered from the flocks at approximately 10 days of age and placed in a common pen where they can be provided with feed and water and protected from competition from normal pen-mates. • Pale colored skin and feather abnormalities. Stunted chicks will grow slowly. A wide range of pathogens can be isolated from affected flocks. Affected birds show decreased pigmentation of the skin which is evident on the shanks and beak. there is no definitive laboratory diagnostic procedure. Enlargement of the pancreas may be noted.

with at least half of this dietary contribution in the form of selenomethionine.1 to 0. Inactivated reoviral vaccines administered during the late rearing period should contain antigenic components which are known to be protective against the reovirus strains (1733) considered responsible for stunting-malabsorption syndrome.• selenium level should range from 0.8 Prevention It is recommended that parent-level pullets receive an attenuated reoviral arthritis vaccine at 7 days followed by a multivalent live vaccine during the 14 to 30 day period consistent with the immunization program for the area. • vitamin E supplementation should conform to NRC levels for stressed flocks (20 IU/kg) All supplementary fats and animal byproducts should be stabilized with 300-600 ppm ethoxyquin or an equivalent compound.3 ppm. 27.
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.

4 Clinical Signs Coccidiosis is generally acute in onset and is characterized by depression.2 Occurrence and Economic Significance Coccidiosis occurs world-wide and is a major cause of mortality and suboptimal growth and feed conversion efficiency in immature flocks unless appropriate preventive measures are implemented. Oocysts can be transmitted mechanically on the clothing and footwear of personnel. mycotoxins) • suboptimal inclusion of anticoccidials or incomplete distribution (poor mixing) in feed. necatrix: severe distention of the mid-jejunum with hemorrhages in the mucosa and red-stained fluid in the lumen. The cost of anticoccidial feed additives and treatment is estimated to exceed $400 million annually in all poultry producing areas of the world. and diarrhea. Birds infected with E. inadequate ventilation. recovered chickens shed oocysts representing a problem in multi-age operations. 28.1 Etiology Various Eimeria spp which parasitize specific portions of the intestinal tract of chickens. maxima: distention of the mid-jejunum with hemorrhages in the mucosa.0 COCCIDIOSIS 28. tenella: hemorrhagic typhlitis (inflammation of the cecum).5 Lesions E. or in some cases. IBD.3 Transmission The sporulated oocyst is the infective stage of the life-cycle. contaminated equipment. inoperative feeding systems. • immunosuppression (Marek’s disease. acervulina and E. 28.28. Infected. E. • environmental and managemental stress such as overstocking. E. tenella show pallor of the comb and wattles and blood-stained cecal droppings. 28. Factors contributing to outbreaks of clinical coccidiosis include:• litter moisture content exceeding 30% due to ingress of rain or leaking waterers. mivati: 1-2mm areas of hemorrhage interspersed with white foci visible through the serosa of the distal duodenum and proximal jejunum. ruffled plumage.
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. 28. E. by wind spreading poultry-house dust and litter over short distances.

Future control measures will include in ovo vaccination of broiler embryos with a highly purified oocyst suspension (Inovocox®). obviating the need for anticoccidials.
102. Severe Eimeria tenella infection showing hemorrhagic ceca.diligent management and monitoring especially if the vaccine is applied over feed.
101. Administration of a vaccine (Coxabic®) derived from gametocytes to replacement pullets has been shown to confer immunity to progeny. Intraocular administration by spray or the insertion of a gelatine cylinder impregnated with oocysts in the chick delivery box contributes to an even distribution of vaccine through the flock. Careful examination of intestinal tracts from at least 5 clinically normal sacrificed birds per flock is necessary to monitor for coccidiosis. (Courtesy AAAP)
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.

proximal and distal to the cecal bifurcation.103. This condition is associated with concurrent Clostridium perfringens enterotoxemia leading to necrotic enteritis. W.
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. AAAP slide set). mivati infection showing white foci visible through the serosa of the duodenum. (Courtesy of Dr.
105. Obvious distention and hemorrhage of the ileum (middle of the intestinal tract) due to infection with Eimeria necatrix.
104. These lesions should be distinguished from the changes caused by Eimeria maxima. Severe Eimeria brunetti lesion in the intestine. Lesions of either Eimeria acervulina or E. Malcolm Reid.

In extreme cases NE is characterized by extensive pseudomembranous enteritis which resembles a coarse yellow coating. Chickens with botulism show ascending paresis and then paralysis extending craniad from the legs. Pathogenic strains of C. an enterotoxemia resulting in progressive paralysis. overstocking. or saturation of litter. Chickens affected with NE develop rigor (“stiffness”) within 1 hour of death. movement or weighing of flocks.29. There are no characteristic lesions associated with botulism. 29. ruffled plumage and extension of the nictitating membrane over the cornea. Terminally affected birds are in sternal recumbency with flaccid necks.1 Etiology Clostridium perfringens is the principal pathogen responsible for necrotic enteritis (NE) although the condition is multi-factorial in origin and is usually preceded by mild intestinal coccidiosis. Successive flocks in some regions show frequent or persistent outbreaks possibly due to high levels of Clostridium spp in soil or the presence of drug-resistant strains. Clostridium botulinum is responsible for botulism.5 Pathology The mucosa of the intestine shows changes ranging from focal hyperemia (redness) to mucosal ulceration.3 Transmission Clostridium perfringens and C. vaccination. perfringens may be introduced onto farms by deficiencies in hygiene and biosecurity. but erosive losses of up to 4% can occur in broiler and immature breeder flocks due to direct mortality or concurrent infection with systemic bacteria. Necrotic enteritis is often initiated by an alteration in the feeding program (commencing skip-a-day feeding of replacement breeder pullets or accidental starvation) environmental stress. Ingestion of the vegetative form of the organisms invariably result in colonization of the intestinal tract. botulinum are ubiquitous soil contaminants. withdrawing anti-coccidial growthstimulating feed additives. 29.4 Clinical Signs Mortality is acute with no specific prodromal or clinical signs. 29.0 CLOSTRIDIAL ENTEROTOXEMIA 29. The economic significance of clostridial enterotoxemia varies. 29. Focal hepatic necrosis may be observed.2 Occurrence and Economic Significance Both NE and botulism can occur world-wide. impairing locomotion.
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. in areas where chickens are reared on litter.

virginamycin or penicillin for 72 hours reduces morbidity and mortality.
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. 29. 29. lincomycin .29. or virginamycin to feed at levels approved by local regulatory authorities will suppress the clinical occurrence of clostridial infections. perfringens can be isolated and identified by a suitably equipped laboratory using anaerobic culture.5 ml of serum into susceptible mice using the intraperitoneal route. Cl. Toxin results in paralysis and death within 24 hours.7 Treatment Administration of flocks with water soluble zinc bacitracin. lincomycin.8 Prevention Addition of zinc bacitracin. Botulinum toxin can be identified in the blood of severely affected broilers by injecting 0. Losses may reoccur following withdrawal of treatment.6 Diagnosis Histological examination of affected mucosa will demonstrate the presence of characteristic clostridial organisms applying Gram stain. Botulism and NE can be prevented by the management procedures recommended to prevent coccidiosis.

Mucosal thickening and focal enteritis occurs with C. galli infection may reduce egg production in floorhoused breeders and commercial layers.1 Capillariasis Infection of the crop (Capillaria contorta) and the intestine (Capillaria obsignata) will result in severe emaciation and mortality in both immature and producing flocks. especially if severe infestation is exacerbated by malnutrition or immunosuppression. contorta.0 ENDOPARASITES 30. or ivermectin (where permitted) in drinking water.5 cm nematode beneath the mucosa (koilin layer) of the ventriculus. Ingluvitis (inflammation of the crop) is associated with C. Death may occur due to intestinal obstruction in birds which are immunosuppressed or are affected by an intercurrent debilitating condition. Syngamus trachea – a 2 cm ( ) nematode in the trachea.5 cm ( ) nematode beneath the nictitating membrane of the eye.3 Cestodiasis Numerous cestode species may occur in the intestinal tract and can be diagnosed at postmortem or by examination of feces. Extensive A. Cestodiasis results in emaciation in mature flocks. obsignata. Other nematodes which may be encountered in subsistence or small-scale flocks include: Oxyspirum mansoni – a 1. Treatment Fenbendazole in feed or levamisole or ivermectin (where permitted) in drinking water. which reveal characteristic bi-operculated ova. Cheilospirura hamulosa – a 2.
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.30. Treatment Piperazine. 30.2 Ascaridiasis Ascaridia galli occurs in the jejunum and Heterakis gallinarum in the cecum. Parasitism can be diagnosed by examination of mucosal scrapings and fecal flotation. In floor-housed breeders and commercial layers reduction in egg production occurs. Tetrameres americana – a 3 mm ( ) spherical nematode beneath the mucosa of the proventriculus. levamisole. 30.

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. Mildly affected chickens show stunting and enlargement of the hock joint with reduction in the length of the leg bones. sometimes with displacement of the gastrocnemius tendon. Chondrodystrophy is characterized by a high prevalence in the flock. • Riboflavin (vitamin B2) deficiency results in a deformity of the feet termed “curled toe paralysis”. • Manganese deficiency results in chondrodystrophy. • Choline and pyridoxine deficiency may result in bilateral enlargement of hock joints. • Chondrodystrophy should be differentiated from valgus-varus abnormality of genetic origin.31.1 Nutritional Etiology • Calcium or phosphorus deficiency or an imbalance in these nutrients will result in rickets in immature birds or osteomalacia in mature breeders and commercial egg-production flocks. • Vitamin D3 (cholecalciferol) deficiency results in rickets in immature flocks housed in controlled environment units. • Thiamine (vitamin B1) deficiency results in an abnormal gait progressing to recumbency and paralysis with hyperextension of the neck. This occurs in growing chicks due to decreased formation of bone below the growth plates of the tibiotarsus and tarsometatarsus. Confirmation of the diagnosis requires analysis of feed to determine manganese content. bilateral involvement of the hock joints and reduction in length of the long bones. • Pyridoxine (vitamin B6) deficiency results in abnormal gait and convulsions. Dietary level should range from 80 to 120 ppm for optimal growth.0 SKELETAL DEFORMITIES AND ARTHRITIS 31. This condition can also occur following administration of toxic levels of nitrofurans to immature flocks. The lesion progresses to severe deformation of the hock joint culminating in displacement of the gastrocnemius (Achilles) tendon (perosis).

The condition can be diagnosed by serology (ELISA or plate agglutination test for flock screening. synoviae. C.2. bending of the tibiotarsus. Riddell.2 Infectious Etiology 31. Under commercial conditions. Lateral spread from infected carrier chick occurs. Lesions of rickets showing. refer to the mycoplasmosis section under respiratory diseases. Transmission Vertical transmission is the principal route of infection. For information on diagnosis. and hemagglutination inhibition for confirmation) or identifying the organism in synovial fluid by culture or by applying PCR technology. Occurrence and Economic Significance Viral arthritis occurs world-wide and is responsible for losses in both commercial broilers and replacement breeding stock. 31. (Courtesy of Dr. Clinical Signs Affected birds aged approximately 30 days onwards show an increasing prevalence of lameness characterized by unilateral or bilateral arthritis of
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. distortion of the ribs and enlargement of the costocondral junctions.113.2 Reoviral Arthritis Specific serotypes (S1133 and WVU 2937) are responsible for arthritis and tenosynovitis. treatment and control of M.1 Mycoplasmosis Mycoplasma synoviae results in serous arthritis.2. indirect transmission is possible through contaminated equipment and from improperly cleaned housing. especially during the first 48 hours after hatch. AAAP slide set)
31.

Occurrence and Economic Significance The condition occurs world-wide but is a problem in specific broiler breeder flocks subject to immune suppression or previous exposure to reoviral arthritis. at mid-cycle.the hock and stifle joints. following reoviral arthritis or mycoplasmosis. This should be followed by a second dose of less-attenuated vaccine at approximately 30 to 40 days of age. High levels of biosecurity including operation of all-in all-out placement programs will prevent lateral transmission. Retrospective serological diagnosis is based on ELISA assay of serum from acute phase and recovered flocks. Prevention Breeding stock and broilers should be obtained from parent flocks immunized against reoviral arthritis. Breeding flocks should be immunized at approximately 4-5 days of age with a mild attenuated reoviral arthritis vaccine administered by the parental route. especially involving the hock and gastrocnemius tendon. Up to 10% of the flock may be affected and lame birds generally die from dehydration or persecution.2. High levels of parental immunity for breeders is stimulated by administration of an inactivated emulsion vaccine prior to point of lay. The extent of the lesion progresses from acute inflammation to chronic fibrosis.3 Staphylococcal Arthritis Etiology Staphylococcus aureus is a primary pathogen but often occurs as an opportunist.
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. 31. Chronic cases show fibrosis of the tendon sheaths which can be palpated in birds which have recovered from the infection. Diagnosis The causal organism can be isolated from synovial (joint and tendon) fluid. Rupture of the tendon occurs in severe cases. and if required. Histopathology of affected tissues shows lymphocytic infiltration and reticular cell proliferation. and may be responsible for losses in hens at onset of sexual maturity. Pathology Both serous arthritis and teno-synovitis are observed.

aureus. synoviae. and is not cost effective. aureus as a secondary infection. 31. is multi-factorial in etiology. Diagnosis Diagnosis is based on isolation and identification of S. Treatment Parental administration of antibiotics to infected birds is only palliative. to reduce the probability of direct inoculation with S. Predisposing factors include wet litter and obesity. Immunosuppressive disease should be controlled by appropriate biosecurity including isolation of flocks and vaccination of breeders. from 40 weeks of age onwards. Prevention Purchase of Ms-free stock and effective vaccination against reoviral arthritis will reduce the occurrence S. Pathology Affected joints yield purulent.
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.3 Pododermatitis Etiology This condition which occurs in mature broiler breeders. Culling of crippled birds is recommended. aureus. Needles used to vaccinate flocks should be sterilized before use and after administering vaccine to 50 consecutive birds. Affected birds invariably die of dehydration and persecution. Occurrence and Economic Significance Pododermatitis is responsible for lameness resulting in death and lowered fertility in broiler breeder flocks. Clinical Appearance Increasing incidence of lameness occurs from 8 to 16 weeks and losses may attain 20% of the flock. aureus occurs through skin abrasions and lacerations and is often a consequence of parenteral vaccination with contaminated needles or contact with improperly cleaned equipment used for weighing. Affected birds are characterized by unilateral or bilateral hock arthritis and occasionally pododermatitis. Concurrent diagnostic procedure should include serology and culture to determine the possibility of previous exposure to reovirus or M. Acceptable biosecurity procedures including decontamination of houses and equipment are recommended.Transmission Introduction of S. viscous yellow or green exudate.

The incidence of pododermatitis has decreased in the USA since the introduction of separate male and female feeding systems for broiler breeders. manganese. Pododermatitis is characterized by gross enlargement of the foot pad. The initial lesion is a superficial erosion which progresses to ulceration of the plantar skin with abscessation and chronic fibrosis of underlying synovial structures. Ionophore toxicity results in paresis and paralysis in chicks. • Water should conform to acceptable standards of purity and mineral content.4% to 0.1 Alleviation of Locomotory Problems Through Nutrition Changes in dietary formulation will alleviate specific nutritional deficiencies but will have no effect on genetic. iron. free of ammonia reduces damage to foot pads. It is advisable to review formulations. Pathology The lesion is characterized histologically by fibrosis.5% available phosphorus for immature flocks.Clinical Appearance Males are more frequently affected than females. (Usually 1. Implementing post-peak feed restriction is necessary to restrict the weight of both males and females within limits recommended by the supplier of breeding stock. • Anticoccidial levels must conform to accepted inclusion rates. • Vitamin premixes should contain acceptable levels of potent D3. biotin. Areas requiring specific attention include:• Calcium and phosphorus levels in the diet should be in accordance with breed specifications. • Trace mineral premixes should contain adequate levels of zinc.
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.0% calcium and 0. Prevention Dry litter. 31.3.) • Limestone should have less than 3% magnesium content. • Ingredients should not contain mycotoxins at toxic levels. and riboflavin. • Essential amino acid content must conform to breed specifications. environmental or infectious causes of locomotory abnormalities. quality control of ingredients and feed in the event of acute episodes of locomotory dysfunction involving a high proportion of a flock. presumably due to their relatively higher weight.

120. Valgus and varus deformities are genetic in origin but severity may be influenced by intercurrent nutritional and managemental factors.4. The condition can be detected at approximately 3 weeks of age and progresses from angular deformation to displacement of the gastrocnemius (Achilles) tendon. Riddell.31. 31. C.5% to 2% of broilers in otherwise normal flocks. The long bones (tibiotarsus and tarsometatarsus) show obvious defects in 0.1 Twisted Legs Valgus (x-legged) and Varus (bow-legged) deformities occur in rapidly growing broilers. AAAP slide set)
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. (Courtesy of Dr. Tibial dyschondroplasia lesion in the proximal end plate of the tibiotarsus.4.4 Developmental Etiology 31. Generally they are not regarded as a significant cause of losses.2 Rotated Tibia and Crooked Toes These changes are observed in turkeys and heavy broilers and are probably genetic in origin.

5 to 1.7 Prevention Immunization is recommended in endemic areas using a mild-attenuated avipox. black scab-like lesions.0 mm diameter. 32.0 AVIAN POX 32. 32. In areas where early exposure occurs.2 Occurrence and Economic Significance The disease occurs in most countries with warm and humid climates.6 Diagnosis Cutaneous lesions are characteristic. Infection of susceptible mature commercial-egg and breeder flocks results in a decline in production. These foci enlarge to become 0. Broilers are frequently affected by the diphtheritic form of the infection.32. 32. 32. 32.4 Clinical Signs Pink focal lesions occur on the comb and wattles and non-feathered portions of the body. which persist for up to two weeks followed by desquamation and healing. chicken-strain virus vaccine administered at approximately 8 weeks of age. Direct intraflock transmission by contact between infected and susceptible birds may occur. The diphtheritic form is recognized by the presence of nodular hyperplasia of the mucosa of the pharynx and trachea. 32. Chickens which die of diphtheritic pox may show a plug of desquamated epithelium which lodge in the glottis resulting in asphyxiation.5 Pathology Histological examination shows characteristic intracytoplasmic inclusion bodies in infected skin and tracheal mucosa.3 Transmission The virus is mosquito-borne. Losses are associated with a depression in growth rate and downgrading due to dermatitis although avian pox does not result in primary mortality. Mild respiratory rales (sounds) may occur in broiler flocks especially with suboptimal ventilation due to tracheitis. Broilers may show confluent and extensive lesions of the back especially in the slow-feathering males of the autosexing strains. the age of vaccination
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. Histological examination of affected tissue will confirm the presence of intracytoplasmic inclusions (Bollinger bodies) in the respiratory mucosa and skin.1 Etiology: An avipoxvirus.

Focal lesion of avian pox on the comb of a hen. broilers are routinely vaccinated against avian pox by subcutaneous injection at day-old. In areas where flocks are affected with vertically transmitted mycoplasmosis. In some areas. adverse vaccine reaction from avian pox vaccine can be prevented by administration of a pigeon-pox vaccine.
121.
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.can be advanced. The efficacy of this procedure is questionable based on demonstrated maternal antibody interference.

33.1 Mites Ornithonyssus spp remain on chickens permanently. Cages and housing can be treated with 2 . The gross appearance of the lesion is pathognomonic. Mature adults are evident on examination.7% carbamate suspension administered by spray. 33.0 ECTOPARASITES 33. The diagnosis may be confirmed by microscopic examination of detritus from scales 33. Only approved insecticides should be applied to poultry or used in the vicinity of housing to avoid contamination of the food chain. Heavy mite infestation is characterized by anemia and the appearance of black mite exoskeleton casts and excreta and dermatitis in the vicinity of the vent.33. Parasitized birds show multiple hematomas associated with feeding sites.
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.5 Treatment Ectoparasites may be treated with a carbamate insecticide such as Sevin®. applied as a 5% powder to birds at two week intervals.2 Argasid Ticks Soft-shelled ticks (Argas spp) occur in tropical areas and may affect cagehoused laying flocks or birds maintained on litter.43 Scaly Leg Mites Chronic infestation of the legs of free-roaming chickens with Knemidocoptes mutans results in proliferation of scales overlying the shanks and feet. Dermanyssus mites parasitize chickens nocturnally. Insecticides should be used in accordance with manufacturers’ label instructions. 33. Lice are responsible for irritation and damage to feathers. Ticks transmit spirochetosis. Egg clusters (“nits”) are observed as spherical white structures adherent to the shafts of feathers.4 Lice Lice are frequently encountered in subsistence flocks. Argasid ticks are nocturnal feeders and favor the soft unfeathered skin beneath the wings.

Blood-sucking Ornithonyssus spp mite. Lice are frequently present in backyard flocks and may depress production if infestation is severe.
123.
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.122. Deposit of louse eggs (“nits”) on the shafts of feathers.
124.

126.
127. Subcutaneous hemorrhage on de-feathered carcass due to nocturnal feeding of Argas spp ticks. Ticks of the genus Argus are vectors of spirochetosis. feather debris. and excreta. Severe infestation with Ornithonyssus spp mites in the region of the vent showing eggs.125.
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.

3 Transmission The fungus is spread by direct contact or by contaminated cages or transport coops. Feather loss may occur if lesions extend to the neck and body of the bird. 34. especially in young birds.34.0 DERMATOMYCOSIS synonyms Favus or “Ringworm” 34.4 Clinical Signs Grey to white scaly lesions appear on the comb and wattles. Histological examination of Gridley-stained tissue will show characteristic hyphae. or 5% formalin will eliminate the infection. Transport crates and other equipment should be thoroughly decontaminated and disinfected to prevent lateral transmission of the agent.2 Occurrence and Economic Significance The condition occurs infrequently in commercial flocks but occurs mainly in subsistence chickens.
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.1 Etiology: Fungi including Trichophyton spp.5 Diagnosis The causal fungus can be cultured from lesions using Sabourauds dextrose agar. 34. 34. 34. spreading progressively.6 Treatment Application of a 2% quaternary ammonium disinfectant. 34. 1% tincture of iodine.7 Prevention Biosecurity precautions should be implemented to avoid introducing infected birds to the flock. 34.

(Courtesy of the University of Georgia)
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.130. wattles. Dermatomycosis (favus or ring worm) characterized by gray scaly appearance of the comb. and nonfeathered areas of the head.

0 MYCOTOXICOSES Mycotoxicosis. and low egg production in breeders and commercial egg flocks.35. Generally.
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. and peanut meal are most frequently implicated in cases of mycotoxicosis. Low levels produce economically significant reduction in growth rate and feed conversion in broilers. suboptimal feed conversion. feed conversion. level of contamination. Immature chickens and ducklings are most susceptible to mycotoxins. low-level mycotoxicoses are difficult to diagnose but should always be considered in cases of a chronic decline in growth rate. Nutrient content of grain is degraded when mold growth occurs on ingredients even in the absence of mycotoxins. The acute and chronic effects of mycotoxins depend on the type of compounds present. Maize with moisture levels over 13% may be contaminated with mycotoxins including aflatoxin. a widespread problem in the poultry industry is caused by ingestion of toxins produced by molds which contaminate cereals and some oilseeds before and subsequent to harvest. ochratoxins. Specific mycotoxins may product characteristic lesions in affected flocks: • Fusarium T-2 toxin is associated with stomatitis (ulceration of the lining of the oral mucosa). and rubratoxins may result in high mortality if lethal levels of these compounds are present in feed. rice. • Chronic aflatoxicosis is responsible for cirrhosis of the liver and ascites. and duration of ingestion. wheat. but age. Aflatoxins. and carcass quality. intercurrent health and environmental stress also influence the response to various toxins in feed. egg production. growth rate. Mycotoxins are a diverse group of chemical compounds which adversely affect liveability. immunosuppression. trichothecenes. • Ochratoxin results in kidney degeneration. egg production or hatchability. Prevention is based on detection of contaminated ingredients and exclusion from diets if this is practical or financially justified. immune response. Maize.

Pale liver of bird receiving 200 ppb aflatoxin in feed (right) compared to liver of bird receiving low level
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.Correct storage of ingredients prevents post-harvest proliferation of molds. Charcoal and clay additives are generally ineffective as mycotoxins binders. Clay compounds may be contaminated with dioxins. Zeolite compounds and extracts from the cell wall of Saccharomyces cerevisiae (Mycosorb®) specifically bind aflatoxin in the intestine. Salvage of feed contaminated with aflatoxin is possible using high temperature ammoniation or adding commercial aluminosilicates to diets.
132. inhibiting absorbtion. Feed additive inhibitors such as propionate and gentian violet will suppress proliferation of fungi and elaboration of toxins. Contaminated corn showing severe fungal infection.
131. Zeolites have limited ability to inactivate other mycotoxins including the fusariotoxins.

Commercial test kits are available to monitor for the presence of mycotoxins. Fred Hoerr)
138. Diarrhea in chick fed fusariotoxin (Courtesy of Dr. Abnormal feather formation (left) due to fusariotoxicosis.
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. Fred Hoerr)
137.136. Compare with normal plumage on right (Courtesy of Dr.

Water proportioner can be used to distribute antibiotics and other medication through the drinking system.
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.139. Monitoring ingredients in feed for the presence of mycotoxins is a necessary quality control procedure.
140. Water proportioners should be calibrated and their operation should be monitored.

36.0 LEUCOCYTOZOONOSIS 36. Clinical signs include depression and decreased feed intake. Gametocytes are elongated structures with prominent nuclei. Exclusion of insect vectors in open-sided houses is impossible. 36.7 Treatment Pyrimethamine in combination with sulfadimethoxine. 36.
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. 36. caulleryi occurs in chickens and L. Muscular incoordination occurs in extremis. Schizonts may be observed in preparations of kidney and liver tissue processed with Romanowski stain.1 Etiology Protozoa of the genus Leucocytozoon. Affected flocks show depressed growth rate and elevated mortality which may be influenced by immuno-suppression and intercurrent primary viral and secondary bacterial infection.2 Occurrence and Economic Significance Leucocytozoonosis is frequently encountered in tropical countries especially where farms are located near lakes or ponds. Introduction of infection into a susceptible breeders or commercial egg-flocks may result in variable reduction in egg production.4 Clinical Signs Flock morbidity may exceed 25% in broilers and replacement egg production flocks.6 Diagnosis Identification of the gametocytes which occur as extra-erythrocytic parasites in stained bloodsmear preparations.8 Prevention Control of insect vectors should be attempted using approved insecticides and draining of standing water. 36. 36.5 Pathology Affected birds show anemia.3 Transmission Leucocytozoon is transmitted by dipterids of the genera Simulium and Culicoides. Batches of ducklings and goslings may show up to 35% mortality. 36. splenomegaly and hepatomegaly. 36. simondi in waterfowl in Asia. L.

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.
NOTE: In many countries.” Malaria caused by Hemaproteus spp are not associated with clinical infections in commercial chickens.Clopidol anticoccidial incorporated in feed at levels ranging from 125 to 250 ppm has been used in the USA to prevent leucocytozoonosis in turkeys.
141. Leucocytozoon parasite visible as extra-erythrocytic structure in Giemsa-stained blood smear. leucocytozoonosis is referred to incorrectly as “malaria.

3 Transmission Duck viral enteritis is transmitted directly by contact of susceptible birds with infected viremic ducks or recovered carriers.4 Clinical Signs Morbidity varies according to the strain of virus and the susceptibility of the flock and may range from 10% to 100% with a corresponding mortality rate. The infection is responsible for severe losses in susceptible flocks. • Hemorrhages of the ovary in mature ducks. 37. tremors of the head and limbs. These signs should be differentiated from botulism. Clinical signs in mature ducks composed paresis. 37. • Hemorrhages of the serosa of the intestine.
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. Affected ducks demonstrate extreme depression.1 Etiology A herpes virus. 37. ruffled plumage.37.5 Pathology Characteristic lesions of duck viral enteritis include: • Free blood in the body cavity. Highly pathogenic strains of the virus may cause hemorrhages from the nares and cloaca.2 Occurrence and Economic Significance Duck viral entertitis occurs in all areas where ducks and geese are raised. Ducks are usually infected from three weeks onwards with an incubation period of 5 to 7 days. Mature breeding flocks show a precipitous decline in egg production immediately preceding a significant rise in mortality. • Free blood in the lumen of the intestine. diarrhea and photophobia. Concentration of ducks in intensive production areas and common use of ponds by commercial flocks and migratory and free-living resident waterfowl predisposes to infection. flaccidity of the neck and terminally. pericardium and capsule of the liver which are evident as petechiae and ecchymoses.0 DUCK VIRAL ENTERITIS synonym “duck plague” DVE 37. 37.

Histological examination discloses the presence of intranuclear inclusion bodies in hepatocytes. Degenerative changes in the intestinal tract extending from the esophagus to the cecum include hemorrhagic areas in the early stages of the disease. commercial ducks should be isolated from free-living waterfowl which are reservoirs of infection. Retrospective diagnosis is based on demonstrating a marked increase in neutralization titers comparing sera from acute. bursa of Fabricius in ducklings and the annular lymphoid bands (gut associated lymphoid tissue) of the intestine. progressing to confluent maculae resembling a diphtheritic pseudomembrane reminiscent of clostridial enteritis in chickens. botulism. 37. 37.6 Diagnosis Characteristic lesions are highly suggestive of the diagnosis. The viral agent can be isolated in 10-day old embryonated duck eggs inoculated by the chorioallantoic route.7 Treatment None.8 Prevention A live attenuated chicken-embryo derived vaccine has been used in Europe to prevent outbreaks. Hemorrhage from nares and also from cloaca is characteristic of DVE. Where possible. It is important to differentiate duck viral enteritis from highly pathogenic avian influenza.
142. newly infected and recovered ducks.Hemorrhagic changes are observed in all lymphoid tissues including the thymus. 37. pasteurellosis and duck viral hepatitis.
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38. virus neutralization in duck embryos and a plaque reduction test to quantify neutralizing antibody.3 Transmission Free-living waterfowl introduce the virus. 38. Mortality is exacerbated by intercurrent bacterial infections. An astrovirus-like agent has been implicated in outbreaks of duck virus hepatitis Type 2 in the UK.1 Etiology A picornavirus is responsible for duck virus hepatitis Types 1 and 3. 38. This agent is distinct from hepadnavirus (duck hepatitis B). In the presence of chlamydiosis or Riemerella spp infection. declining in severity to under 10% at 4 weeks of age.4 Clinical Signs Morbidity in susceptible flocks may range from 50% to 100%.2 Occurrence and Economic Significance Duck virus hepatitis Types 1 and 3 occur in ducklings under 4 weeks of age in all intensive duck-rearing areas of the world.0 DUCK VIRUS HEPATITIS 38.
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. with losses of up to 90% in batches under one week of age. Ducklings demonstrate peracute mortality preceded by lateral recumbency and occasionally. Direct contact between infected and susceptible flocks especially in multiage operations predisposes to disease. opisthotonos (hyperextension of the neck. airsacculitis and peritonitis may be observed. Mortality results in extensive losses especially with intercurrent bacterial infections including chlamydiosis.5 Pathology The significant lesion comprises enlargement of the liver with punctate or ecchymotic hemorrhages. 38. “stargazing”). 38. Rodents serve as reservoir hosts on affected farms. Mortality is dependent on the age of the flock. 38. mycotoxicosis and environmental stress. Riemerella and E. Serologic procedures include agar gel diffusion precipitin test.6 Diagnosis The picoronaviruses responsible for duck virus hepatitis can be isolated from livers using 9-day old embryonated SPF chickens inoculated by the allantoic sac route. coli infection.

Breeders can be immunized with a live attenuated chicken-embryo origin vaccine. Where possible. E. An injection of 0..7 Treatment No specific treatment is available.
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.8 Prevention Hyperimmune serum from flocks surviving duck viral hepatitis can be administered to ducklings. salmonellosis. High mortality in newly placed ducklings has a wide differential diagnosis including DVH. single-age isolated placement programs should be followed. Some vaccines have shown reversion to virulence when applied to large flocks.
143.38. Supportive therapy is recommended. coli.5 ml filtered serum is recommended using the intramuscular route. aspergillosis and mycotoxicosis. Rodents should be eradicated. 38. and Riemerella infection.

resulting in variable morbidity and mortality during the first two weeks of the brooding period.0 DUCKLING SEPTICEMIA 39. 39. 2 and 5 has been developed.
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. 39. 39.4 Clinical Signs Affected ducklings show depression.39. liver or brain tissue on either blood agar or trypticase soy agar. especially in ducklings which display nervous signs. 39. salmonellosis and duck virus hepatitis. Footpad lesions from defective wire floors predispose to percutaneous infection. Enrofloxacin can be administered in drinking water at a level of 50 ppm for the first 2 days followed by 25 ppm for 4 subsequent days. Multivalent or homologous bacterins have been prepared for administration to ducklings at 1 to 2 weeks of age. pericarditis and fibrinous airsacculitis. coli.5 Pathology Septicemic changes characterized by perihepatitis.1 Etiology Riemerella anatipestifer is the principal pathogen responsible for duckling septicemia. A live attenuated vaccine against serotypes 1.6 Diagnosis Diagnosis is based on isolation and identification of Rimerella anatipestifer from heart blood.2 Occurrence and Economic Significance Duck septicemia occurs in all areas where ducklings are reared commercially. avoiding overcrowding and chilling should be implemented. ataxia. septicemia. ocular and nasal discharge and respiratory rales. fibrinous meningitis occur. Concurrent infections include E. In some cases. 39. which is administered to ducklings by the aerosol route or in drinking water at day-old. 39.8 Prevention Managemental interventions including effective sanitation between placements.7 Treatment Supportive therapy and administration of water soluble tetracycline may be attempted.3 Transmission Direct contact of susceptible ducklings with a contaminated environment. 39. hepatomegaly and splenomegaly are observed.

Periodic epornitics have been described in commercial operations.4 Clinical Signs Acute infection in young ducks is characterized by ataxia. 40. including waterfowl.7 Treatment Commercial duck flocks can be treated by administration of
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. attributed to transmission of virulent strains from indigenous or migratory bird species by direct and indirect contact and presumably by insect vectors.1 Etiology Chlamydia psittaci.0 CHLAMYDIOSIS 40.6 Diagnosis Diagnosis is confirmed by isolation of the organism from homogenates of organs obtained using sterile necropsy technique. 40. Laboratory host systems include embryonated eggs inoculated by the yolksac route and mice inoculated by the intraperitoneal route. Infection requires inhalation of viable elementary bodies. 40. Commercial transport and handling of waterfowl previously in contact with ornamental and companion species may result in outbreaks in distribution centers associated with trade in live birds. purulent ocular and nasal discharge. diarrhea. Chronic cases show emaciation and chronic respiratory involvement.3 Transmission The disease is transmitted by both acutely infected birds and latent carriers. 40. 40.5 Pathology Chlamydiosis should be suspected if the following lesions are observed in waterfowl: • Fibrinous pericarditis and perihepatitis • Hepatomegaly and splenomegaly • Airsacculitis 40. This infection is transmitted to humans and is regarded as an important zoonotic infection.2 Occurrence and Economic Significance Outbreaks of chlamydiosis occur in poultry.40. throughout the world. an obligatory intracellular organism. Laboratory techniques include fluorescent antibody detection and retrospective diagnosis using the complement fixation procedure.

It is necessary to follow statutory requirements regarding withdrawal periods following administration of antibiotic before sale or slaughter of flocks. 40.
144. and obligatory reporting of outbreaks. Chlamydiosis should be considered in cases of fibrinous peritonitis and airsacculitis.
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. It is virtually impossible to control chlamydiosis in multiage flocks with the opportunity for direct and indirect contact. free-living Psittacines and Colombibormes.8 Prevention Appropriate biosecurity procedures should be imposed to prevent transmission from infected reservoirs including companion bird species.chlortetracycline in feed at a level of 400 grams per ton for a period of up to two weeks.